This document discusses oncologic emergencies in pediatrics. It begins with an introduction and overview of common pediatric malignancies. It then categorizes oncologic emergencies and discusses several examples in more depth, including metabolic emergencies like tumor lysis syndrome, hematologic emergencies such as hyperleukocytosis and bleeding disorders, and cardiothoracic emergencies like superior vena cava syndrome. For each emergency, it covers pathophysiology, risk factors, diagnostic criteria, evaluation and management strategies. The document provides a comprehensive review of potential life-threatening complications that may arise from pediatric cancers or their treatment and strategies for rapid recognition and management.
This document discusses tumor lysis syndrome (TLS), a metabolic oncologic emergency caused by the breakdown of malignant cells following chemotherapy or radiation therapy. TLS results in the release of potassium, phosphorus, uric acid and other intracellular components into the bloodstream, potentially causing hyperkalemia, hyperphosphatemia, hyperuricemia and other electrolyte imbalances. The document outlines risk factors for TLS, signs and symptoms of specific electrolyte abnormalities, treatment approaches, and importance of monitoring patients at risk.
Management of oncology emergencies, Mohh'd sharshirMoh'd sharshir
This document summarizes the management of oncologic emergencies, focusing on tumor lysis syndrome (TLS). TLS is caused by massive lysis of tumor cells, releasing potassium, phosphate and uric acid. It is classified based on laboratory and clinical criteria. Risk is highest in Burkitt lymphoma, ALL and other high-grade lymphomas. Prevention focuses on IV hydration and hypouricemic agents like rasburicase or allopurinol. Electrolyte abnormalities are managed based on their severity. High-risk patients receive aggressive prevention while intermediate-risk patients generally receive allopurinol prevention.
Oncologic emergencies are vital for many healthcare practitioners to note even if they do not take care of cancer patients alone. This slide deck covers malignant spinal cord compression, hypercalcemia of malignancy, and tumor lysis syndrome.
This document discusses tumor lysis syndrome (TLS), which can occur when tumors undergo rapid cell lysis and release intracellular contents into the bloodstream. TLS can cause electrolyte abnormalities and renal failure. It affects patients with highly proliferative tumors undergoing chemotherapy, radiation or other treatments. The document outlines risk factors, grading criteria, clinical manifestations, prevention strategies including hydration, uric acid reduction and dialysis, as well as treatment of established TLS complications. It also covers hyperleukocytosis, a related condition seen in some leukemia patients.
Central nervous system tumors are the second most common type of cancer in children. 20-25% of childhood cancers are CNS tumors. The most common types are astrocytic tumors such as pilocytic astrocytoma and medulloblastoma. Medulloblastoma is an embryonal tumor that occurs most often in the cerebellum and has a high risk of spreading through the cerebrospinal fluid. Treatment involves maximal surgical resection followed by craniospinal radiation therapy and chemotherapy, with doses and regimens varying based on risk factors like age and extent of resection. Treatment planning for craniospinal irradiation aims to deliver a uniform dose to the entire target volume while minimizing risks of under-
A 60-year-old male laborer presented with a recurrent soft tissue sarcoma on his right proximal arm that had been growing over 7 years. He had previously undergone 3 surgeries and chemotherapy/radiation for the mass. Examination found a large, necrotic mass with normal neurovascular function. Biopsy confirmed a low-grade soft tissue sarcoma. The management plan was a wide excision with reconstruction to remove the recurrent tumor.
This document discusses tumor lysis syndrome (TLS), a metabolic oncologic emergency caused by the breakdown of malignant cells following chemotherapy or radiation therapy. TLS results in the release of potassium, phosphorus, uric acid and other intracellular components into the bloodstream, potentially causing hyperkalemia, hyperphosphatemia, hyperuricemia and other electrolyte imbalances. The document outlines risk factors for TLS, signs and symptoms of specific electrolyte abnormalities, treatment approaches, and importance of monitoring patients at risk.
Management of oncology emergencies, Mohh'd sharshirMoh'd sharshir
This document summarizes the management of oncologic emergencies, focusing on tumor lysis syndrome (TLS). TLS is caused by massive lysis of tumor cells, releasing potassium, phosphate and uric acid. It is classified based on laboratory and clinical criteria. Risk is highest in Burkitt lymphoma, ALL and other high-grade lymphomas. Prevention focuses on IV hydration and hypouricemic agents like rasburicase or allopurinol. Electrolyte abnormalities are managed based on their severity. High-risk patients receive aggressive prevention while intermediate-risk patients generally receive allopurinol prevention.
Oncologic emergencies are vital for many healthcare practitioners to note even if they do not take care of cancer patients alone. This slide deck covers malignant spinal cord compression, hypercalcemia of malignancy, and tumor lysis syndrome.
This document discusses tumor lysis syndrome (TLS), which can occur when tumors undergo rapid cell lysis and release intracellular contents into the bloodstream. TLS can cause electrolyte abnormalities and renal failure. It affects patients with highly proliferative tumors undergoing chemotherapy, radiation or other treatments. The document outlines risk factors, grading criteria, clinical manifestations, prevention strategies including hydration, uric acid reduction and dialysis, as well as treatment of established TLS complications. It also covers hyperleukocytosis, a related condition seen in some leukemia patients.
Central nervous system tumors are the second most common type of cancer in children. 20-25% of childhood cancers are CNS tumors. The most common types are astrocytic tumors such as pilocytic astrocytoma and medulloblastoma. Medulloblastoma is an embryonal tumor that occurs most often in the cerebellum and has a high risk of spreading through the cerebrospinal fluid. Treatment involves maximal surgical resection followed by craniospinal radiation therapy and chemotherapy, with doses and regimens varying based on risk factors like age and extent of resection. Treatment planning for craniospinal irradiation aims to deliver a uniform dose to the entire target volume while minimizing risks of under-
A 60-year-old male laborer presented with a recurrent soft tissue sarcoma on his right proximal arm that had been growing over 7 years. He had previously undergone 3 surgeries and chemotherapy/radiation for the mass. Examination found a large, necrotic mass with normal neurovascular function. Biopsy confirmed a low-grade soft tissue sarcoma. The management plan was a wide excision with reconstruction to remove the recurrent tumor.
1. Oncological emergencies refer to urgent clinical situations in cancer patients caused by cancer or its treatment.
2. Some examples discussed are hypercalcemia, tumor lysis syndrome, lactic acidosis, hypoglycemia, syndrome of inappropriate antidiuretic hormone secretion, superior vena cava syndrome, spinal cord compression, severe cystitis, bladder hemorrhage, disseminated intravascular coagulation, and cardiac tamponade.
3. The document provides details on symptoms, signs, and treatment approaches for each of these conditions.
This document discusses hypercalcemia in malignancy. It begins with an introduction defining hypercalcemia and its prevalence in certain cancers. It then covers normal calcium metabolism regulation involving bone, plasma, vitamin D, and the RANK/RANKL pathway. Etiologies of hypercalcemia in malignancy include PTHrP-mediated humoral hypercalcemia, local osteolytic hypercalcemia, 1,25-dihydroxyvitamin D mediated, and hyperparathyroidism. Clinical presentation involves neurologic, gastrointestinal, cardiovascular, and renal symptoms. Diagnostic evaluation includes calcium levels and approaches based on etiology. Management involves increasing urinary calcium excretion, inhibiting bone resorption with bisphosphonates or den
Oncology and surgical practice are becoming more integrated, as surgeons are often responsible for initially diagnosing and managing solid tumors. A thorough understanding of cancer epidemiology, etiology, staging, and natural history is required to determine the optimal surgical therapy for each patient. Tumor cells acquire several characteristics before becoming fully malignant, including establishing independence from normal growth controls, achieving immortality and angiogenesis, and developing the abilities to invade other tissues and disseminate throughout the body. Both genetic and environmental factors contribute to cancer development in complex ways. A combination of inherited predispositions and exposures to carcinogenic chemicals, viruses, radiation, and other external factors drive the transformation of normal cells into malignant tumors.
Blood is made up of different types of cells like red blood cells (RBC’s), which carries oxygen, platelets which helps in blood clotting and white blood cells (WBC’s) that fight infections. These cells basically comes from stem cells, which have the potential to develop into any type of blood cell as they divide and mature. Problems in this process, known as ‘differentiation’, are at the root of all blood cancers. Different types of blood cancer depend on when and how these problems occur.
This document provides an overview of malignant spinal cord compression (MSCC). It begins with a clinical case of a 56-year-old man initially diagnosed with back pain and sciatica who is later found to have prostate cancer with MSCC. The anatomy of the spinal cord is reviewed, followed by the definition, incidence, symptoms, investigations and treatments of MSCC. Common cancers that cause MSCC are discussed. The document concludes with outcomes of MSCC and NICE guidance recommendations focusing on early detection and urgent treatment.
Tumor lysis syndrome is an oncologic emergency characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia due to the rapid breakdown of tumor cells. It occurs after initiation of chemotherapy or other cytotoxic treatments in cancers with a high proliferative rate or large tumor burden. Prophylaxis includes aggressive hydration and use of urate-lowering agents like allopurinol or rasburicase to prevent uric acid crystal formation and preserve kidney function. Early recognition and treatment are important to prevent complications such as acute kidney injury or life-threatening cardiac arrhythmias.
This document provides an overview of acute myeloid leukemia (AML). It discusses the historical background, classification, clinical features, risk stratification, diagnostic evaluation, and treatment regimens for AML. Key points include that AML is characterized by infiltration of blood and bone marrow by proliferative myeloid cells, the WHO classification system is based on clinical features, morphology, cytogenetics and molecular abnormalities, risk is stratified by cytogenetics and molecular markers, and treatment involves supportive care, induction chemotherapy, and consideration of novel targeted therapies or stem cell transplant depending on risk factors.
This document discusses the management of acute myeloid leukemia (AML). It begins by classifying leukemias and providing statistics on AML incidence and mortality. It then describes the clinical presentation, diagnosis, prognostic factors, treatment including induction chemotherapy and post-remission therapy, and special considerations for acute promyelocytic leukemia. The treatment sections focus on standard "7+3" induction with cytarabine and anthracyclines, achieving remission, and post-remission strategies including high-dose chemotherapy and stem cell transplant depending on risk factors.
Ethics presentation given at Providence Health Care on 2/19/16 as a part of a day-long nursing oncology conference. Discusses the fundamental clinical ethics consultation approach and discusses in narrative the relevant ethics cases that are common to oncology practice
Management of Anemia in cancer patientsAjeet Gandhi
Anemia in cancer patients are important both in terms of quality of life as well as response to therapy. Cause of anemia is multi-factorial and its management is critical in optimizing best outcomes of cancer patients
1. The patient presented with hypercalcemia due to metastatic lung cancer. Symptoms included confusion, dehydration, and signs of renal impairment.
2. Initial management involved IV rehydration with normal saline to improve kidney function and increase calcium excretion. Bisphosphonate therapy was given to reduce calcium levels.
3. Further imaging found a mass in the right hilum and new liver metastasis, consistent with progression of the original lung cancer.
This document provides information on the management of soft tissue sarcoma. It discusses the clinical presentation, patterns of spread, imaging, histology, grading, staging, prognostic factors and management of soft tissue sarcomas. The key points are:
1) Soft tissue sarcomas most commonly present as painless swellings in the extremities and can invade locally along fascial planes. Imaging like MRI is important for assessing tumor extent.
2) Histologically, the most common subtypes are undifferentiated pleomorphic sarcoma and liposarcoma. Grading systems consider tumor differentiation, mitosis and necrosis.
3) Staging is based on tumor size, depth, nodal status and metastasis
The document discusses various oncologic emergencies including metabolic emergencies like tumor lysis syndrome, haematologic emergencies like hyperleukocytosis and coagulopathy, infections like febrile neutropenia and typhlitis, and neurological emergencies like spinal cord compression and increased intracranial pressure. It provides details on the pathophysiology, clinical features, investigations and management of these conditions.
Malignant ascites, an abnormal accumulation of fluid in the abdominal cavity, is commonly associated with cancers like ovarian cancer, gastrointestinal cancers, and breast cancer. It develops due to mechanical obstruction of lymphatic drainage by tumors and increased vascular permeability caused by cytokines. Diagnosis involves abdominal ultrasound or CT scan followed by diagnostic paracentesis of the fluid to examine for malignant cells. Treatment options include dietary salt restriction, diuretics, repeated paracentesis, indwelling catheters, peritoneovenous shunting, and intraperitoneal chemotherapy.
The document discusses several oncological emergencies including tumor lysis syndrome, leucoestasis, hypercalcemia, superior vena cava syndrome, spinal cord compression, and hyperviscosity syndrome. It provides details on the pathogenesis, risk factors, signs and symptoms, diagnostic evaluation and treatment recommendations for each condition. The treatment sections emphasize hydration, uric acid lowering agents, corticosteroids, radiation therapy, surgery, chemotherapy and other supportive measures depending on the specific emergency.
Discuss the principles guiding the use of radiotherapy in surgeryAbdullahi Sanusi
The document discusses the principles guiding the use of radiotherapy in surgery. It covers topics such as the physical and biological basis of radiotherapy, indications and contraindications, treatment planning, technical aspects, and complications. Radiotherapy is an important clinical discipline for treating cancer and some benign diseases. About 60% of cancer patients require radiotherapy during their treatment course. The principles of radiotherapy are based on understanding the physical and biological effects of ionizing radiation on tumors and normal tissues. [END SUMMARY]
Tumor lysis syndrome is caused by massive tumor cell lysis and release of electrolytes into circulation, potentially causing kidney damage. Risk factors include large tumor burden, rapid proliferation, sensitivity to treatment, preexisting kidney conditions, and inadequate hydration or electrolyte control. Prevention focuses on aggressive hydration, uric acid reduction via allopurinol or rasburicase, electrolyte management, and sometimes dialysis for severe cases.
Tumor lysis syndrome is a potentially life-threatening condition caused by the rapid breakdown of tumor cells during cancer treatment, releasing electrolytes into the bloodstream. It can cause severe electrolyte abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These abnormalities are due to the release of intracellular contents from dying tumor cells and can lead to acute kidney injury. Tumor lysis syndrome is most common in patients with high-grade lymphomas and leukemias undergoing aggressive chemotherapy and requires careful monitoring and prevention with hydration and medications to reduce complications.
1. Oncological emergencies refer to urgent clinical situations in cancer patients caused by cancer or its treatment.
2. Some examples discussed are hypercalcemia, tumor lysis syndrome, lactic acidosis, hypoglycemia, syndrome of inappropriate antidiuretic hormone secretion, superior vena cava syndrome, spinal cord compression, severe cystitis, bladder hemorrhage, disseminated intravascular coagulation, and cardiac tamponade.
3. The document provides details on symptoms, signs, and treatment approaches for each of these conditions.
This document discusses hypercalcemia in malignancy. It begins with an introduction defining hypercalcemia and its prevalence in certain cancers. It then covers normal calcium metabolism regulation involving bone, plasma, vitamin D, and the RANK/RANKL pathway. Etiologies of hypercalcemia in malignancy include PTHrP-mediated humoral hypercalcemia, local osteolytic hypercalcemia, 1,25-dihydroxyvitamin D mediated, and hyperparathyroidism. Clinical presentation involves neurologic, gastrointestinal, cardiovascular, and renal symptoms. Diagnostic evaluation includes calcium levels and approaches based on etiology. Management involves increasing urinary calcium excretion, inhibiting bone resorption with bisphosphonates or den
Oncology and surgical practice are becoming more integrated, as surgeons are often responsible for initially diagnosing and managing solid tumors. A thorough understanding of cancer epidemiology, etiology, staging, and natural history is required to determine the optimal surgical therapy for each patient. Tumor cells acquire several characteristics before becoming fully malignant, including establishing independence from normal growth controls, achieving immortality and angiogenesis, and developing the abilities to invade other tissues and disseminate throughout the body. Both genetic and environmental factors contribute to cancer development in complex ways. A combination of inherited predispositions and exposures to carcinogenic chemicals, viruses, radiation, and other external factors drive the transformation of normal cells into malignant tumors.
Blood is made up of different types of cells like red blood cells (RBC’s), which carries oxygen, platelets which helps in blood clotting and white blood cells (WBC’s) that fight infections. These cells basically comes from stem cells, which have the potential to develop into any type of blood cell as they divide and mature. Problems in this process, known as ‘differentiation’, are at the root of all blood cancers. Different types of blood cancer depend on when and how these problems occur.
This document provides an overview of malignant spinal cord compression (MSCC). It begins with a clinical case of a 56-year-old man initially diagnosed with back pain and sciatica who is later found to have prostate cancer with MSCC. The anatomy of the spinal cord is reviewed, followed by the definition, incidence, symptoms, investigations and treatments of MSCC. Common cancers that cause MSCC are discussed. The document concludes with outcomes of MSCC and NICE guidance recommendations focusing on early detection and urgent treatment.
Tumor lysis syndrome is an oncologic emergency characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia due to the rapid breakdown of tumor cells. It occurs after initiation of chemotherapy or other cytotoxic treatments in cancers with a high proliferative rate or large tumor burden. Prophylaxis includes aggressive hydration and use of urate-lowering agents like allopurinol or rasburicase to prevent uric acid crystal formation and preserve kidney function. Early recognition and treatment are important to prevent complications such as acute kidney injury or life-threatening cardiac arrhythmias.
This document provides an overview of acute myeloid leukemia (AML). It discusses the historical background, classification, clinical features, risk stratification, diagnostic evaluation, and treatment regimens for AML. Key points include that AML is characterized by infiltration of blood and bone marrow by proliferative myeloid cells, the WHO classification system is based on clinical features, morphology, cytogenetics and molecular abnormalities, risk is stratified by cytogenetics and molecular markers, and treatment involves supportive care, induction chemotherapy, and consideration of novel targeted therapies or stem cell transplant depending on risk factors.
This document discusses the management of acute myeloid leukemia (AML). It begins by classifying leukemias and providing statistics on AML incidence and mortality. It then describes the clinical presentation, diagnosis, prognostic factors, treatment including induction chemotherapy and post-remission therapy, and special considerations for acute promyelocytic leukemia. The treatment sections focus on standard "7+3" induction with cytarabine and anthracyclines, achieving remission, and post-remission strategies including high-dose chemotherapy and stem cell transplant depending on risk factors.
Ethics presentation given at Providence Health Care on 2/19/16 as a part of a day-long nursing oncology conference. Discusses the fundamental clinical ethics consultation approach and discusses in narrative the relevant ethics cases that are common to oncology practice
Management of Anemia in cancer patientsAjeet Gandhi
Anemia in cancer patients are important both in terms of quality of life as well as response to therapy. Cause of anemia is multi-factorial and its management is critical in optimizing best outcomes of cancer patients
1. The patient presented with hypercalcemia due to metastatic lung cancer. Symptoms included confusion, dehydration, and signs of renal impairment.
2. Initial management involved IV rehydration with normal saline to improve kidney function and increase calcium excretion. Bisphosphonate therapy was given to reduce calcium levels.
3. Further imaging found a mass in the right hilum and new liver metastasis, consistent with progression of the original lung cancer.
This document provides information on the management of soft tissue sarcoma. It discusses the clinical presentation, patterns of spread, imaging, histology, grading, staging, prognostic factors and management of soft tissue sarcomas. The key points are:
1) Soft tissue sarcomas most commonly present as painless swellings in the extremities and can invade locally along fascial planes. Imaging like MRI is important for assessing tumor extent.
2) Histologically, the most common subtypes are undifferentiated pleomorphic sarcoma and liposarcoma. Grading systems consider tumor differentiation, mitosis and necrosis.
3) Staging is based on tumor size, depth, nodal status and metastasis
The document discusses various oncologic emergencies including metabolic emergencies like tumor lysis syndrome, haematologic emergencies like hyperleukocytosis and coagulopathy, infections like febrile neutropenia and typhlitis, and neurological emergencies like spinal cord compression and increased intracranial pressure. It provides details on the pathophysiology, clinical features, investigations and management of these conditions.
Malignant ascites, an abnormal accumulation of fluid in the abdominal cavity, is commonly associated with cancers like ovarian cancer, gastrointestinal cancers, and breast cancer. It develops due to mechanical obstruction of lymphatic drainage by tumors and increased vascular permeability caused by cytokines. Diagnosis involves abdominal ultrasound or CT scan followed by diagnostic paracentesis of the fluid to examine for malignant cells. Treatment options include dietary salt restriction, diuretics, repeated paracentesis, indwelling catheters, peritoneovenous shunting, and intraperitoneal chemotherapy.
The document discusses several oncological emergencies including tumor lysis syndrome, leucoestasis, hypercalcemia, superior vena cava syndrome, spinal cord compression, and hyperviscosity syndrome. It provides details on the pathogenesis, risk factors, signs and symptoms, diagnostic evaluation and treatment recommendations for each condition. The treatment sections emphasize hydration, uric acid lowering agents, corticosteroids, radiation therapy, surgery, chemotherapy and other supportive measures depending on the specific emergency.
Discuss the principles guiding the use of radiotherapy in surgeryAbdullahi Sanusi
The document discusses the principles guiding the use of radiotherapy in surgery. It covers topics such as the physical and biological basis of radiotherapy, indications and contraindications, treatment planning, technical aspects, and complications. Radiotherapy is an important clinical discipline for treating cancer and some benign diseases. About 60% of cancer patients require radiotherapy during their treatment course. The principles of radiotherapy are based on understanding the physical and biological effects of ionizing radiation on tumors and normal tissues. [END SUMMARY]
Tumor lysis syndrome is caused by massive tumor cell lysis and release of electrolytes into circulation, potentially causing kidney damage. Risk factors include large tumor burden, rapid proliferation, sensitivity to treatment, preexisting kidney conditions, and inadequate hydration or electrolyte control. Prevention focuses on aggressive hydration, uric acid reduction via allopurinol or rasburicase, electrolyte management, and sometimes dialysis for severe cases.
Tumor lysis syndrome is a potentially life-threatening condition caused by the rapid breakdown of tumor cells during cancer treatment, releasing electrolytes into the bloodstream. It can cause severe electrolyte abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These abnormalities are due to the release of intracellular contents from dying tumor cells and can lead to acute kidney injury. Tumor lysis syndrome is most common in patients with high-grade lymphomas and leukemias undergoing aggressive chemotherapy and requires careful monitoring and prevention with hydration and medications to reduce complications.
Tumor lysis syndrome is a potentially life-threatening condition caused by the rapid breakdown of tumor cells during cancer treatment, releasing electrolytes into the bloodstream. It can cause severe electrolyte abnormalities like hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. These abnormalities are due to the release of intracellular contents from dying tumor cells and can lead to acute kidney injury. Tumor lysis syndrome is most common in patients with high-grade lymphomas and leukemias undergoing aggressive chemotherapy and requires careful monitoring and prevention with hydration and medications to avoid complications.
Tumor Lysis Syndrome
The most common disease-related emergency encountered by physicians caring for children or adults with hematologic cancers
When tumor cells release their contents into the bloodstream, either spontaneously or in response to therapy-
leading to the characteristic findings of
hyperuricemia, hyperkalemia, hyperphosphatemia, and
hypocalcemia
Electrolyte and metabolic disturbances- progress to clinical toxic effects- including
-renal insufficiency,
-cardiac arrhythmias,
-seizures, and
-death due to multiorgan failure
Laboratory tumor lysis syndrome : Requires that two or more of the metabolic abnormalities occur within 3 days before or up to 7 days after the initiation of therapy
Clinical tumor lysis syndrome: Laboratory tumor lysis syndrome is accompanied by an increased creatinine level, seizures, cardiac dysrhythmia, or death.
IN MALIGNANCIES
–high proliferative rate,
–large tumor burden,
–high sensitivity to treatment-
Initiation of cytotoxic chemotherapy,
Cytolytic antibody therapy,
Radiation therapy,
Sometimes glucocorticoid therapy alone
Rapid lysis of tumor cells!!!!!
Releases massive quantities of intracellular contents:
K+ , phosphate, and nucleic acids
AKI is common in cancer patients and associated with increased hospital costs and length of stay. A large Danish study found the incidence of AKI to be 17.5% within one year and 27% within five years in cancer patients. AKI in cancer patients can result from the cancer itself, cancer treatments, or associated conditions like sepsis. Tumor lysis syndrome is an oncology emergency caused by massive tumor cell lysis releasing potassium, phosphate, and nucleic acids, resulting in electrolyte abnormalities and renal failure. Prevention focuses on aggressive intravenous hydration and use of uric acid-lowering agents like allopurinol or rasburicase. Patients must be closely monitored for signs of TLS after starting cancer treatment.
Tumor lysis syndrome (TLS) describes metabolic derangements that occur from rapid tumor breakdown associated with cytotoxic therapy. It is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. TLS requires immediate intervention as it can overwhelm homeostatic mechanisms. It occurs primarily in hematologic malignancies with high proliferation rates that are sensitive to therapy. Prevention through hydration, hypouricemic agents, and monitoring of at risk patients is important to manage TLS.
Tumor lysis syndrome occurs when cancer cells release their contents into the bloodstream, causing electrolyte imbalances like hyperkalemia, hyperuricemia, and hyperphosphatemia that can damage organs. It is diagnosed when a patient develops acute kidney injury, arrhythmias, or seizures from their electrolyte changes. Treatment involves rapid hydration, uric acid-lowering drugs like allopurinol or rasburicase, and dialysis for severe electrolyte abnormalities or kidney injury. With advances in prevention and management, the prognosis for tumor lysis syndrome has improved in recent years.
Tumor lysis syndrome occurs when malignant cells are rapidly lysed, releasing cellular contents into the bloodstream and overwhelming the body's ability to process them. This causes electrolyte abnormalities like hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. It is commonly seen after chemotherapy for hematologic cancers and treated with aggressive hydration, uric acid-lowering drugs like allopurinol or rasburicase, and dialysis for acute kidney injury. Early identification of at-risk patients allows for prophylactic measures to prevent complications.
Tumor lysis syndrome describes the clinical and laboratory abnormalities that result from the rapid release of intracellular contents from dying tumor cells. It is a common oncologic emergency seen by nephrologists. The rapid release of ions and metabolites causes hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Prevention focuses on identifying at-risk patients and aggressive hydration and urate-lowering agents. Treatment involves fluid management, management of electrolyte abnormalities with agents like rasburicase, and potentially renal replacement therapy for severe cases.
This document provides information about tumor lysis syndrome (TLS), including its definition, risk factors, pathophysiology, and management. TLS is an oncometabolic emergency that can occur after tumor targeted therapy leads to rapid cell death and release of cellular contents like uric acid, potassium, and phosphorus. It can cause abnormalities in electrolytes and kidney injury. High risk groups include those with hematologic malignancies like lymphoma. Management involves prevention, monitoring, volume expansion, and in some cases urinary alkalinization or allopurinol.
The document discusses tumor lysis syndrome (TLS), a potentially fatal metabolic complication that can result from spontaneous or treatment-related tumor cell death. TLS is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. It defines TLS and outlines its frequency, etiology, risk factors, pathophysiology, prevention, diagnosis, and management, emphasizing the importance of identifying high-risk patients and initiating preventive treatment to avoid complications like acute renal failure.
Onconephrology shield the kidney while fighting cancer , dr ayman seddikAyman Seddik
This document discusses kidney diseases that can occur in patients with cancer or undergoing cancer treatment. It begins by defining onconephrology as the field of nephrology dealing with kidney complications of cancer. Common reasons a nephrologist may be consulted include kidney diseases that predate or develop during cancer, new glomerular diseases, obstructive nephropathy, tubular damage, thrombotic microangiopathy, radiation nephropathy, tumor invasion of the kidney, tumor lysis syndrome, and electrolyte disorders. Kidney complications discussed in more depth include acute kidney injury, cancer-associated glomerulopathy, chemotherapy-associated tubulointerstitial nephritis, hypercalcemia of
Tumor lysis syndrome (TLS) is a metabolic complication that can occur when large numbers of malignant cells are rapidly destroyed, releasing their intracellular contents into the bloodstream. This disrupts electrolyte levels and can damage organs like the kidneys, heart, and brain. TLS is treated with intravenous fluids, medications to lower uric acid, phosphate, and potassium levels, and sometimes dialysis. Patients at highest risk are those with highly chemosensitive tumors undergoing new chemotherapy. Close monitoring and preventative measures like hydration and anti-hyperuricemic drugs before and after treatment can help reduce risks of TLS in at-risk patients.
This document discusses oncological emergencies, including tumor lysis syndrome, malignant hypercalcemia, superior vena cava syndrome, and others. It provides details on the definitions, causes, clinical presentations, diagnostic criteria, and treatment approaches for these time-sensitive cancer complications. Tumor lysis syndrome can result from cell lysis releasing uric acid and electrolytes, and requires aggressive hydration, allopurinol or rasburicase, and renal replacement therapy if severe. Malignant hypercalcemia is most common in breast and lung cancers and multiple myeloma, presenting with nausea, fatigue, and neurological symptoms, treated initially with hydration and bisphosphonates. Superior vena cava syndrome ob
Tumor lysis syndrome is an oncologic emergency caused by massive tumor cell lysis and release of potassium, phosphate, and nucleic acids. It is defined and graded based on laboratory and clinical criteria. Patients at high risk include those with high tumor burden and bulky disease, high white blood cell counts, and impaired renal function. Prevention focuses on aggressive hydration, uric acid-lowering agents like allopurinol and rasburicase, and monitoring. Established TLS is treated with electrolyte management, rasburicase, diuretics, and possibly renal replacement therapy. Close monitoring of electrolytes, creatinine, and uric acid is important for both prevention and management of this potentially life
This document discusses hypercalcemia and hypocalcemia, including their causes, symptoms, and management. Hypercalcemia can be caused by hyperparathyroidism, certain malignancies, vitamin D toxicity, and other conditions. Symptoms range from none in mild cases to fatigue, nausea, and cognitive issues in severe cases. Treatment focuses on rehydration, bisphosphonates, calcitonin, surgery, and addressing the underlying cause. Hypocalcemia is usually asymptomatic but can cause tingling and seizures in severe cases. It is often caused by hypoparathyroidism, vitamin D deficiency, or tumor lysis syndrome. Treatment involves calcium and vitamin D supplementation to address the deficiency. Laboratory tests are important to
1. Oncological emergencies include life-threatening events in cancer patients caused by the malignancy or its treatment.
2. Common oncological emergencies include tumor lysis syndrome, hypercalcemia of malignancy, febrile neutropenia, and superior vena cava syndrome.
3. Tumor lysis syndrome occurs due to the rapid release of intracellular contents from dying tumor cells, causing electrolyte abnormalities. Hypercalcemia of malignancy is most commonly caused by parathyroid hormone-related protein overproduction. Febrile neutropenia is a common complication of chemotherapy. Superior vena cava syndrome involves extrinsic compression of the superior vena cava.
This document provides an overview of acute rheumatic fever presented by Dr. Renesha Islam. Some key points:
- Acute rheumatic fever is an immune response to Group A streptococcus infection that causes inflammation of the heart, joints, brain and skin. It often damages the heart valves long term.
- Major symptoms include migratory polyarthritis in joints (75% of cases), carditis (50-60% of cases, involving the heart valves, myocardium and pericardium), Sydenham's chorea (10-15% of cases), erythema marginatum and subcutaneous nodules (rare).
- Diagnosis is based on the revised Jones criteria
Importance of examination of Pulse & BP in children.pptxDr. Renesha Islam
This document provides information on examining pulse and blood pressure in children. It discusses what pulse is, how to take a pulse in different locations like the radial artery and brachial artery, and how to assess pulse rate, rhythm, volume, and character. It describes abnormal pulse findings like tachycardia, bradycardia, irregular rhythms, and abnormal pulse characters. It explains factors that can cause variations in pulse examination and outlines important information that can be learned from assessing the pulse.
The document provides information on evaluating a neonate presenting with cholestatic jaundice. It discusses taking a thorough history and conducting a physical exam. Important investigations include liver function tests to establish cholestasis and assess severity, and tests to identify treatable conditions like infection or galactosemia. Imaging like ultrasound and hepatobiliary scintigraphy can differentiate between extrahepatic and intrahepatic causes. A liver biopsy further aids diagnosis and management of neonatal cholestasis. Common etiologies include biliary atresia, idiopathic neonatal hepatitis, and metabolic disorders. Timely evaluation is important to diagnose treatable conditions and avoid unnecessary surgery.
This document provides details of a clinical meeting presentation about a 2 year 4 month old boy named Saif who was admitted with a 2.5 month history of fever and 2 month history of chest pain and breathing difficulty. On examination, he was mildly pale with enlarged lymph nodes and hepatomegaly. Imaging showed a left-sided pleural effusion. A biopsy revealed T-cell lymphoblastic lymphoma. He received supportive treatment and chemotherapy according to the BFM-95 protocol. On follow up, he was improving with continued chemotherapy and a repeat chest x-ray showed improvement in the pleural effusion.
This document provides an overview of hemophagocytic lymphohistiocytosis (HLH). It begins by introducing HLH and describing its characteristics such as fever, hepatosplenomegaly, and cytopenias. It then discusses the classification of primary and secondary HLH, epidemiology, genetic causes, clinical features, diagnostic guidelines, treatment protocols, and long-term follow up recommendations. For the patient presented, the document recommends following the HLH-2004 treatment protocol initially and considering continuation therapy or stem cell transplant depending on the disease response and severity.
Sadia, a 10-year old girl, presented with pain and swelling in her left leg for 3 months and difficulty walking for 1 month. She also had a new painless swelling near her left eye. Initial workup found a mass in her left leg and another in her left eye area. Biopsies of the masses found features suggestive of Ewing sarcoma and metastatic neuroblastoma. Further imaging and testing confirmed the diagnosis of metastatic neuroblastoma with a primary tumor in her left leg and metastases in her left eye area.
- Genotyping plays an important role in the diagnosis and management of thalassemia. Laboratory diagnosis requires tests like complete blood count, hemoglobin electrophoresis, and DNA analysis to identify mutations.
- Over 1,800 mutations have been identified, with several common ones in different regions. Genotype also influences disease severity, with some mutations causing milder forms when combined with alpha-thalassemia.
- Several techniques can be used for DNA analysis including allele-specific PCR, reverse dot-blot, Sanger sequencing, and next-generation sequencing. While more advanced methods like NGS improve accuracy, considerations like cost must be made. Overall, genotyping aids in precise diagnosis, treatment decisions and genetic
Alfi, a 10-year old boy, presented with sudden onset of severe pallor, dark colored urine, and jaundice. Examination found severe pallor, jaundice, splenomegaly, and otherwise normal vital signs. Initial workup showed features of hemolysis, positive direct Coombs test, and elevated bilirubin and LDH. The provisional diagnosis was autoimmune hemolytic anemia, which was confirmed. Treatment with steroids led to improvement in symptoms and laboratory values over subsequent follow ups.
This presentation contains all the updated information regarding ongoing treatment protocol, HSCT, Antibiotic prophylaxis, upcoming targeted therapies related to AML
The document provides information about an upcoming seminar on thalassemia. It includes details about the presenters and two case scenarios that will be discussed. It also provides background information on thalassemia including epidemiology, genetics, clinical presentation, complications, diagnosis, and management. The key topics that will be covered in the seminar are outlined.
This document discusses various modalities for treating cancer including chemotherapy. It provides details on the mechanisms of action, goals and classifications of different chemotherapeutic agents. It describes how certain drugs like methotrexate, cyclophosphamide and cisplatin directly damage DNA to inhibit cell proliferation. It also discusses concepts like drug resistance, cell cycle specificity and overcoming resistance through combination therapy. The document concludes by summarizing adverse effects of major drug classes and approaches to manage toxicities.
Dr. Renesha Islam and Dr. Farzana Alam Mou presented on retinoblastoma. The presentation included an overview of retinoblastoma including its: anatomy and histology; classification based on laterality, focality, heredity, family history and growth pattern; genetics involving mutations in the RB1 gene; clinical presentations; investigations including examination under anesthesia and imaging; treatment options; and prognosis. Retinoblastoma is a malignant tumor of the retina that predominantly affects young children.
The document discusses megaloblastic anemia in a 13-year-old boy who was admitted with symptoms of fever, pallor, weakness, and numbness. It provides details on the patient's lab results showing macrocytosis, hypersegmented neutrophils, and reduced vitamin B12 levels. The presenters then discuss the causes, clinical features, investigations, diagnosis, and management of vitamin B12 and folate deficiency megaloblastic anemias.
Dr. Renesha Islam and Dr. Farzana AlamMou presented two cases of pediatric patients with bleeding and low platelet counts. The first case was a 5-year-old boy, Yasin, with petechiae and bleeding who had a platelet count of 35,000/cmm. The second case was a 13-year-old girl, Asma, with ecchymosis and menorrhagia who had a platelet count of 20,000/cmm. The doctors then discussed immune thrombocytopenia, including its history, pathophysiology involving autoantibodies and impaired platelet production, classification as acute or chronic, and clinical manifestations ranging from no symptoms to severe bleeding.
Jubair, a 12-year-old boy, was admitted with fever, pallor, blackish spots on the body, gum bleeding, and blood in stool. Examination found pallor, gum swelling, and enlarged liver and spleen. Tests showed low blood cell counts, elevated D-dimer and fibrinogen levels. Bone marrow biopsy found 60% promyelocytes. Immunophenotyping and genetic testing confirmed the diagnosis of acute promyelocytic leukemia (APL). APL is a type of acute myeloid leukemia characterized by a genetic mutation and abnormal promyelocytes. It requires emergent treatment including all-trans retinoic acid (ATRA) to induce differentiation and prevent potentially fatal
This document provides an outline for a seminar on arterial blood gas analysis (ABG). The seminar will include an introduction to ABGs, indications for ordering ABGs, the procedure for arterial blood sampling, pulmonary gas exchange, acid-base disorders, and how to approach analyzing an ABG. Resident doctors from pediatrics and cardiology will present on these topics and discuss ABGs versus venous blood gases.
Immunization of children with cancer is a burning topic. Not only concerned parents but also paediatric oncologists have so many questions and queries regarding this matter. This presentation will try to answer those questions with the help of recent and updated guidelines on immunization of both developed and developing countries.
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
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Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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3. ONCOLOGIC EMERGENCY
Any acute, potentially life threatening event, either
directly or indirectly related to a patient’s cancer or
its treatment, which if not anticipated, quickly
recognized & effectively treated, may rapidly result
in permanent morbidity or death of the patient.
Importance:-
o Need to be addressed before therapy can begin or
continue.
o To avoid end-organ injury.
4. Pediatric Malignancies
Adapted from: American Cancer Society Cancer Facts & Figures, 2007. Atlanta, American Cancer Society, 2007.
Leukemia, 30%
CNS, 22.3%
Other, 17.1%
Neuroblastoma, 7.3%
Wilms, 5.6%
Rhabdo, 3.1%
HL, 3.5%
NHL, 4.5%
Osteo, 2.4%
Rb, 2.8%
Ewing’s, 1.4%
5. • To facilitate recognition and management,
emergencies are categorized in following way-
o Metabolic
o Haematologic
o Cardiothoracic
o Abdominal
o Genitourinary
o Neurological
o Endocrine
o Treatment related emergencies &
o Miscellaneous.
6. METABOLIC EMERGENCIES
• Tumor lysis syndrome (TLS) and associated
electrolyte derangements.
• Hypercalcaemia
• Syndrome of inappropriate anti diuretic
hormone secretion (SIADH)
• Shock.
7. TUMOR LYSIS SYNDROME
TLS arises due to the rapid release of intracellular
metabolites (such as phosphorous, potassium & uric
acid) from dying tumor cells in quantities that exceed
the excretory capacity of the kidneys.
• Although it can occur prior to any cytotoxic therapy,
its manifestations usually appear 12 to 72 hours from
the initiation of therapy.
More common in:
Lymphoproliferative tumors with abdominal
involvement (e.g. B cell/ T cell Iymphoma, leukaemias
and Burkitt's Iymphoma)
10. Risk Factors for the Tumor Lysis Syndrome
CATEGORIES OF RISK FACTORS
1.CANCER MASS:-
Bulky tumor or extensive metastasis
Organ infiltration by cancer cells
Bone marrow involvement
Renal infiltration or outflow-tract
obstruction
2. CELL LYSIS POTENTIAL:-
High rate of proliferation of
cancer cells
Cancer-cell sensitivity to
anticancer therapy
Intensity of initial anticancer
therapy
3. FEATURES ON PATIENT PRESENTATION
Nephropathy before diagnosis of
cancer
Dehydration or volume depletion
Acidic urine
Hypotension
Exposure to nephrotoxins
4. SUPPORTIVE CARE
Inadequate hydration
Exogenous potassium
Exogenous phosphate
Delayed uric acid removal
11. Risk Factors for the Tumor Lysis Syndrome
Risk Factor Comment
Bulky tumor or
extensive metastasis
The larger the cancer mass or the higher the number of
cells that will lyse with treatment, the higher the risk of
clinical tumor lysis syndrome.
Organ infiltration by
cancer cells
Hepatomegaly, splenomegaly, and nephromegaly generally
represent tumor infiltration into these organs, and
therefore a larger tumor burden than that of patients
without these findings.
Bone marrow
involvement
Healthy adults have 1.4 kg of bone marrow.
A marrow that has been replaced by leukemic cells
contains a cancer mass greater than 1 kg and therefore
represents bulky disease.
Renal infiltration or
outflow-tract
obstruction
Decreased urine flow predispose to nephropathy from
other causes, such as the tumor lysis syndrome.
1. Cancer mass:-
12. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
High rate of
proliferation of
cancer cells
Lactate dehydrogenase level is a surrogate for tumor
proliferation.
The higher the level, the greater the risk of the tumor lysis
syndrome.
Cancer-cell
sensitivity to
anticancer therapy
Cancers that are inherently more sensitive to therapy have
a higher rate of cell lysis and a greater risk of the tumor
lysis syndrome than the other cancers.
Intensity of initial
anticancer therapy
Preexisting nephropathy from hypertension, diabetes, gout,
or other causes has a greater risk for acute kidney injury
and the tumor lysis syndrome.
2. Cell lysis potential:-
13. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Nephropathy before
diagnosis of cancer
Urine flow predispose to nephropathy from other causes,
such as the tumor lysis syndrome.
Dehydration or
volume depletion
Dehydration decreases the rate of urine flow through renal
tubules and increases the level of solutes
Acidic urine Uric acid has a lower solubility in acidic urine and therefore
crystallizes more rapidly
Hypotension Hypotension decreases urine flow and increases the level of
solutes that can crystallize. Hypotension can also
independently cause acute kidney injury.
Exposure to
nephrotoxins
Vancomycin, aminoglycosides, contrast agents for diagnostic
imaging, and other potential nephrotoxins increase the risk
of acute kidney injury from lysis of cancer cells.
3. Features on patient presentation:-
14. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Inadequate
hydration
Increases the risk of crystallization inside tubules
Exogenous
potassium
Unless the patient has severe hypokalemia or a
dysrhythmia from hypokalemia, potassium should not
be included in the intravenous fluids, and potassium
(from food or medications) should be minimized until
the risk period for the tumor lysis syndrome has
passed.
4. Supportive care:-
15. Risk Factors for the Tumor Lysis Syndrome.
Risk Factor Comment
Exogenous phosphate Restricting dietary phosphate and adding a phosphate
binder reduce the exogenous load of phosphate so that the
kidneys need only excrete the endogenous load of
phosphate released by cancer-cell lysis.
Delayed uric acid
removal
Allopurinol prevents formation of new uric acid by inhibiting
xanthine oxidase and preventing conversion of xanthine to
uric acid. It does not remove existing uric acid and does
increase urinary excretion of xanthine, which can crystallize
and cause nephropathy. Rasburicase is an enzyme that
rapidly removes uric acid by converting it to allantoin,
which is highly soluble and readily excreted in the urine.
The longer the uric acid level remains high, the greater the
risk of crystal formation and acute kidney injury.
4. Supportive care:-
16. Diagnostic Criteria for Laboratory & Clinical TLS
• Laboratory TLS (LTLS): The presence of two or more
abnormal serum values at presentation. Such as-
• Clinical TLS (CTLS): Presence of LTLS and one or more
of the following clinical complications: renal
insufficiency, cardiac arrhythmias, seizures or sudden
death.
MetabolicAbnormality Laboratory level
Hyperuricemia S. uric acid ≥8 mg/dl
Hyperphosphatemia S. Phosphate ≥6.5 mg/dl (2.1 mmol/L)
Hyperkalemia S. K+ ≥6.0 mmol/L
Hypocalcemia S. Ca+ ≤7.0 mg/dl (≤1.75 mmol/L)
S. Creatinine >normaL
17. Evaluation and Diagnosis
Close attention to symptoms of
electrolyte abnormalities
Laboratory investigation
– Abdominal pain, Fullness
– Back pain
– Vomiting
– Anorexia, Cramps
– Diarrhoea
– Signs of dehydration
– Muscle spasms
– Tetany, seizures
– Diminshed urine output
-CBC
-S. Electrolytes
-S. Ca
-S. Phosphate
-S. Uric acid
-LDH
-ECG
18. MANAGEMENT
• Hydration: 2–4 times maintenance fluid.
Maintain urine output >100 mL/m2/hr
Urine specific gravity <1.010
5% Dextrose in 0.25% Normal saline
No K+, Ca+, PO4.
• Alkalinization:
40-80 mEq/L to maintain urine pH 7.0–7.5
Increase NaHCO3 as needed
Stop NaHCO3 when cytotoxic therapy is initiated
or the urine pH >7.5 or S. TCO2 reaches 30mEq/L.
19. MANAGEMENT
• Diuresis: If U/O poor (< 60ml/m2/hr)
Avoid if hypovolemia present
Furosemide (0.5–1.0 mg/kg)
Mannitol (0.5 g/kg over 15 min) --if patient
has oliguria, unresponsive to increased hydration and
furosemide.
• Uric acid reduction:
Allopurinol 300 mg/m2/day or 10mg/kg/day PO
Rasburicase (recombinant urate oxidase)-
0.15-0.2mg/kg/day IV, for 1 or 2 days
The dose can be repeated.
21. TLS Management - Hyperkalemia
Mild (< 6 mEq/l) and asymptomatic:
Hydration and diuretics.
Kayexelate(1g/kg+ 50% sorbitol)
Moderate to severe:
-Rapid insulin (0.1 U/kg/h) plus
glucose (dextrose 0.5 g/kg/h)
- Life-threatening arrhythmias IV calcium gluconate
(100-200 mg/kg) or calcium chloride (10 mg/kg)
- NaHCO3 (1-2 mEq/kg IV)
- Dialysis
CAN BE FATAL
K+=
22. TLS Management - Hypocalcemia
• Only treat if symptomatic
– Fatigue, cramping, tetany, laryngospasm, weakness,
paresthesias, Seizure, ECG changes.
• Control Phos Level
– PO4 binders
• CaCl2
– 10 mg/kg IV
• Ca Gluconate
– 100 mg/kg IV
Hall and Todd, Postgrad Med J, 2006
23. • Hyperphosphatemia: Low phosphate diet & Hydration
Aluminum hydroxide (150 mg/kg/day)
• Transfusion: If indicated.
• Dialysis: Indicated in-
-Progressive renal failure with K+ > 6 mEq/l, PO4 > 10 mg/dl
-Persistent hyperkalemia with QRS interval widening
-Severe metabolic acidosis.
-Volume overload unresponsive to diuretic therapy.
-Anuria and overt uremic symptoms (i.e., encephalopathy).
-Severe symptomatic hypocalcemia.
-Hypertension (BP150/90) and inadequate U/O at 10 hr from
start of treatment.
-Congestive heart failure.
MANAGEMENT
24. Patients at high risk for the tumor lysis syndrome may also
receive low-intensity initial therapy.
– Slower lysis of the cancer cells allows renal homeostatic
mechanisms to clear metabolites before they
accumulate and cause organ damage.
– This strategy, in cases of advanced B-cell non-Hodgkin’s
lymphoma or Burkitt’s leukemia, has involved treatment
with low-dose cyclophosphamide, vincristine, and
– prednisone for a week before the start of intensive
chemotherapy. Similarly, many groups subscribe to a
week of prednisone monotherapy for childhood acute
lymphoblastic leukemia.
PREVENTION OF ACUTE
KIDNEY INJURY
27. Hyperleukocytosis & Leukostasis
• Peripheral leukocyte count >100 000/ml
• Clinically significant if- > 200,000/mL in AML,
> 300,000/mL in ALL & CML
• May be asymptomatic or may present with-
Mental status change, headache, blurred vision,
dyspnoea, cyanosis, dactilytis seizure, stroke, coma.
• May lead to death by-
-CNS Hemorrage
-Pulmonary Leukostasis
-Metabolic derangements that accompany tumor lysis.
29. Mechanism:
• High number of blasts in microcirculation ⇒ sludging ⇒
interferes with oxygenation of local tissue ⇒ Tissue
Ischemia
• Adhesive reaction between abnormal vascular
endothelium & the circulating blasts worsening
leukostasis, thrombosis ⇒ secondary hemorrhage.
•Higher metabolic rate of blasts & local production of
cytokines ⇒ Tissue hypoxia.
•Thrombi in the circulation ⇒ vascular damage &
parenchymal ischemia ⇒ pulmonary or cerebrovascular
hemorrhage & edema.
30. Management of Hyperleukocytosis
Hydration
•To facilitate excretion of toxic metabolites
•To reduce blood viscosity
Alkalinization
Allopurinol/Urate oxidase
Avoid ↑ blood viscosity
•Cautious use of blood transfusion and diuretics.
Exchange transfusions/ leukopheresis.
Ultimate Rx- Systemic anti-cancer chemotherapy
initiated soonest possible.
31. BLEEDING IN THE CANCER PATIENT
Third most common cause of death after organ failure
due to tumor invasion and infection.
Thombocytopenia
Coagulation abnormality
Effect of other drugs-mucositis caused by cytotoxic
drugs or corticosteroids.
Acute GIT Bleeding-hematemesis & melena.
Massive Hemoptysis
Oral Bleeding
Epistaxis.
32. DIC
• Microthrombi &
bleeding
– Platelet & clotting
factor consumption
– Microangiopathy
– Hyperfibrinolysis.
• Etiologies
– Gram -ve sepsis
– Leukemia (AML M3,M5;
ALL with high WBC)
– Metastatic solid tumors.
Semin Thromb Hemost. 2007 33(4):408-15
www.medscape.com
Sepsis/
Malignancy
Systemic
activationof
coagulation
Widespread
intravascular
fibrin
deposition
Consumption
of plts,
clotting
factors
Severe
Bleeding
Thrombosis,
organ
failure
33. DIC -Management
• Anticipation, frequent lab/clinical monitoring.
• Replace consumed factors
– Platelets: Transfuse to keep > 50K initially
– Fibrinogen: FFP or Cryo to keep > 150 mg/dL
– No routine use of heparin or antifibrinolytics.
• Treat underlying cause
– AML: Start chemo
– APML: Start ATRA as soon
as suspected
– Sepsis: Antibiotics.
34. Depression Of Bone Marrow Activity
Depression of normal bone marrow activity
results in –
-Anaemia
-Thrombocytopenia and
-Neutropenia.
Treated with supportive care, regardless of their
etiology.
Supportive care often includes transfusion of
individual blood components.
35. Cardiothoracic Emergencies
o Superior vena cava syndrome & superior
mediastinal syndrome
o Pleural & pericardial effusion
o Cardiac Temponade
o Pneumothorax & pneumomediastinum
o Massive Hemoptysis
o ATRA syndrome.
36. CVCS & SMS
• consists of the S/S of superior vena
cava (SVC) obstruction due to
compression or thrombosis.
• Pathophysiology:
– Compression, obstruction of SVC
– Thin wall, low intraluminal
pressure
– Impaired venous return.
Superior mediastinal syndrome(SMS)
consists of SVCS with tracheal
compression.
-Airways more compliant and
compressible in children.
38. Chee et al., Nature Clinical Practice
Cardiovascular Medicine, 2007
39. Diagnosis should be made quickly by least invasive
procedure.
1. Chest radiography
2. CT Scan
3. CBC, Serum LDH, Uric acid, α-fetoprotein, β-HCG
4. ECG
5. If possible, a tissue specimen for diagnosis
Several reports suggest a stepwise approach to
diagnosis.
If tolerated
40. SVCS/SMS CXR MASS
Non diagnostic Diagnostic
Generate D/Ds
Assess risk
Anesthesia Low
risk
Anesthesia High
risk
Biopsy Treat
Re-assess
Treat
Treat
Low risk Biopsy Treat
High risk Treat
CBC, other studies
41. o Establishing a tissue diagnosis may not be possible &
patients may need empiric Rx as a life-saving measure.
1st-line treatment in emergent situations is high-dose
steroids (Prednisolone or Methylprednisolone).
Patient should undergo biopsy as soon as the mass
shrinks & the patient is stable.
o If poor response to steroids
chemotherapy such as vincristine, cyclophosphamide
with or without an anthracycline can be added.
Therapy
42. If a solid tumor not responsive to steroids or
chemotherapy
Emergent radiation can be performed.
For symptomatic venous thrombosis with no
evidence of hemorrhage
• Anticoagulation can be initiated using systemic or
low-molecular-weight heparin (LMWH)
46. Evaluation & Diagnosis
• Pain is the principal symptom : detail history regarding
Location, quality & timing,
Relation to status of cancer
Recent medication
Surgical history
• Observation and a gentle examination-
Whether the child lies still
Winces with cough, movement or motion
Distension, asymmetry, surgical scar
Rectal examination.
47. Investigations
Serial CBC
Blood Culture
Serum Electrolytes
Abdominal X-ray ( supine, erect and left
lateral decubitus)
Chest X-ray
Endoscopic and Colonoscopic examination
Imaging Studies : Abdominal US, CT, MRI
48. Typhlytis/ Neutropenic Enterocolitis
Necrotizing colitis typically localised to terminal ileum
and caecum. May progress from inflammation to full
thickness infraction and perforation.
Caused by : Pseudomonas species, E. coli &
other Gram (-)ve bacteria, Staphylococcus, alpha-
hemolytic Streptococcus, Clostridium, Candida and
Aspergillus.
Occurs in : 6% of Acute leukaemia cases common in
AML, but also in ALL, HSCT recipient.
51. Neutropenic Colitis
• Thickened cecum
• Peri-intestinal soft-tissue stranding
• Free Fluid
• Pneumatosis Intestinalis
Van de Wetering, Supp Care Can, 2003
www.meddean.luc.edu
radiology.rsna.org
52. Treatment
In the past mortality was 20% to almost 100%
But now, 70% - 80% pt can be managed medically.
Nothing per oral
N-G suction
Broad spectrum Antibiotic to cover gram (-)ve,
Clindamycin or Metronidazole for anaerobes, and anti-
fungal
IV fluid and Electrolytes
Tranfusion of PRBC & platelet
Vasopressin (as needed)
53. Proposed criteria for surgical intervention
Persistent gastro-intestinal bleeding despite resolution
of thrombocytopenia and coagulation abnormalities.
Evidence of free air.
Need for vasopressor support or large volumes of
fluid.(Suggestive of uncontrolled sepsis from intestinal
infraction)
Development of symptom of an intra-abdominal
process that would normally require an operation.
56. .
• Evaluation
• BUN, creatinine, electrolytes.
• Close monitoring of all intake and output.
• CT or ultrasound (US) of abdomen/pelvis.
57. Treatment
Vigorous hydration for prerenal etiologies including BK
viremia.
• Decompression of obstructed kidney with stenting or
catheter placement.
• Treatment of underlying tumor with chemotherapy,
surgery, or radiation to decrease outflow obstruction.
• Avoidance of nephrotoxic agents.
• With significant electrolyte abnormalities, fluid
overload or true anuria, consideration of dialysis may be
indicated.
58. .
Definition
• Systolic or diastolic blood pressure outside the
95th percentile for age, gender, and height.
Etiology
• Secondary to pain or anxiety, and often transient.
• Secondary to tumor compression of renal
parenchyma leading to increased renin production
(secondary hyperaldosteronism).
• Secondary increased renin production from tumors
(e.g., pheochromocytoma, Wilms’ tumor,
neuroblastoma)
Hypertension
60. ‘
• Nicardipine (0.51 μg/kg/min infusion to be titrated to
desired blood pressure).
• Labetalol (0.21 mg/kg/dose IV, to be avoided in
patients with bronchospasm or diabetes).
• Sublingual nifedipine (510 mg/dose for children
weighing .10 kg).
• Oral clonidine (0.050.1 mg/dose).
Chronic hypertension:
• Amlodipine (0.1 mg/kg per dose, or 2.55 mg/day).
• Consider ACE inhibitors or beta-blockers.
Hypertension from fluid overload:
• Furosemide (0.51 mg/kg)
61. .
Signs and symptoms of hemorrhagic cystitis are
hematuria caused by bleeding and inflammation of
the bladder, leading to dysuria, urgency, and
frequency. Substantial blood loss and urinary
obstruction can result.
• Therapy with CPM and IFOS are the most common
causes of hemorrhagic cystitis.
• The early phases of hemorrhagic cystitis are mucosal
edema, ulceration, epithelial necrosis, and submucosal
fibrosis. Long-term complications include bladder
fibrosis and contraction, urinary reflux, renal failure,
and transitional cell bladder tumors..
Hemorrhagic Cystitis
62. .
The diagnosis is made by
• History and urinalysis.
• Ultrasonography
Treatment:
Chemotherapy-induced cystitis is best prevented by
vigorous hydration and brisk diuresis.
Concurrent use of the uroprotective agent sodium-2-
mercaptoethanesulfonate (MESNA)
Antiviral.
67. Spinal Cord Compression
3-5% of children with cancer develop acute spinal cord or
cauda equina compression. Sarcomas account for about half
of the cases of spinal cord involvement in childhood.
Pathophysiology
The most common scenario for cord compression is the
direct extension of a metastatic lesion from the vertebrae
into the epidural space
The most common site of compression is the thoracic
spine (70%). The lumbar spine 20%, cervical spine10%.
Clinical Presentation
Back pain with localized tenderness occurs in 80% of
patients.
Incontinence, urinary retention, and other abnormalities
of bowel or bladder function.
68. .
• Loss of strength and sensory deficits with a sensory level
may occur.
Evaluation
A thorough history and neurologic examination.
Spinal radiographs, MRI
Cerebrospinal fluid analysis
Treatment:
It is crucial to initiate treatment immediately.
Dexamethasone is initiated to decrease local edema,
prior to diagnostic studies.
If an epidural mass is identified, treatment is aimed at
rapid decompression. Chemotherapy, radiation therapy,
or surgical decompression may be used.
69.
70. Causes:
brain tumours e.g. astrocytoma, disseminated
subarachnoid tumor, Pseudotumor cerebri, APL
treated with ATRA, and with Abscesses, massive
cerebrovascular accidents , CNS hemorrhage, and
extensive meningeal tumor.
Signs and symptoms vary according to age/site.
Infant: vomiting, lethargy, regression of milestones,
seizures, symptoms of obstructive hydrocephalus.
Older: early morning recurrent headaches with or
without vomiting.
Cerebellar: Ipsilateral hypotonia and ataxia
Herniation of cerebellar tonsil – head tilt and neck
stiffness.
Increased ICP and brain herniation
71. .
Tumors near 3rd ventricle – visual loss, ICP and
hydrocephalus - obstruction of aqueduct of Sylvius due
to pineal tumour – ICP & Parinaud’s syndrome.
Evaluation and Treatment
Emergent CT scan is the radiologic study of choice than
MRI.
ICP should receive dexamethasone (1st dose, 1 to 2
mg/kg, then 0.25 to 0.5 mg/kg every 6 hours)
Acute manifestations of herniation (altered
consciousness and respiratory or circulatory collapse)
from increased ICP require mannitol (0.5 to 1 g/kg IV
over 30-60 minutes).
Removal of the mass lesion is the definitive therapy for
increased ICP.
72. .
Tumor
Primary central nervous system
tumor
Metastatic tumor
Leukemic meningitis
Hyperleukocytosis
Central nervous system
infection
Viral
Bacterial
Fungal
Protozoal
Cerebrovascular accident
Etiology of Seizures in Children with Cancer
Treatment
Intrathecal methotrexate
Intrathecal cytosine arabinoside
L-Asparaginase. Others, hypoxia.
73. Cerebrovascular accident
Direct or metastatic spread of tumour,
antineoplastic agent, haematologic abnormality.
L-Asparaginase associated with venous or lateral and
sagittal sinus thrombosis caused by rebound
hypercoagulable state
AML especially APML associated with CVA. Due
to release of procoagulant.
• Management
Suportive
Use of anticoagulant potentially
detrimental
In L-Aspa induced, recommended FFP
75. .
Etiology
1. Involves continuous pituitary release of antidiuretic
hormone (ADH)
2. Results from physiologic stress, pain, surgery,
mechanical ventilation, infections, CNS and pulmonary
lesions, lymphomas, and leukemias.
4. Occurs as a side effect of vincristine, vinblastine,
cyclophosphamide, ifosfamide, cisplatin, and melphalan.
5. Occurs in overhydration with hypotonic fluids,
diabetes insipidus with free water replacement, and
cerebral salt wasting.
Syndrome of Inappropriate Antidiuretic
Hormone Secretion (SIADH)
76. .
Clinical Features
• Oliguria,Weight gain,fatigue, headache, and nausea.
• Late manifestations include lethargy, confusion,
hallucinations, seizures, and coma.
Laboratory Features of SIADH
• Low serum osmolality (,280 mOsm/l).
• High urine osmolality (.500 mOsm/l).
• Urine to serum osmolality ratio >1.
• Hyponatremia (sodium, ,130 mEq/l).
• Increased urine specific gravity.
77. .
Treatment
1.Fluid restriction.
2. Furosemide 1 mg/kg should be administered.
3. Hydration with normal saline limited to insensible
losses (500 ml/m2/24 h) plus ongoing losses.
4. severe neurologic involvement (seizures or coma),
hydrate carefully with hypertonic saline 3%
78. Associated with Non Hodgkin & Hodgkin Lymphoma.
Rare in children.
Ca+ > 12mg/dl – Affect multiple organ system.
> 20mg/dl- Fatal.
• S/S: Nausea, constipation, polyuria, profound muscle
weakness, bradyarrhythmias, renal insufficiency, coma.
• Treatment:
- Excretion: Hydration, Forced diuresis
- Mobilization: Prednisone (acts slowly)
Calcitonin
Biphosphonates
-Treatment of the malignancy.
Hypercalcaemia
79. Adrenal Insufficiency
• Etiology
1.Secondary to significant prior
corticosteroid exposure.
2. During periods of critical
illness, trauma, surgery, or
infection.
3. Tissue resistance to steroids.
4. Adrenal gland failure.
Clinical Features
1. Fatigue, dizziness,
weakness, myalgia,
nausea/vomiting.
2. Severe hypotension,
shock.
3. Hyponatremia,
hyperkalemia, metabolic
acidosis with normal anion
gap
80. .
• 1. Glucocorticoid replacement therapy
(hydrocortisone): a. Hydrocortisone
b. Strict monitoring for hyperglycemia
• 2. Treatment includes interventions for sepsis and
hypotension .
• 3. Consider checking cortisol levels as patient may
need physiologic replacement once stress dosing is
complete
Treatment
82. .
1. Discontinue inciting agent.
2. Maintain vascular access & Assess respiratory status.
3. If bronchospasm or hypotension: a. IM epinephrine
(0.01 mg/kg of 1:1000 dilution b. IV fluid boluses with
normal saline are recommended. c. Persistent wheezing,
consider albuterol and prepare for intubation.
4. H1 blockers
5. H2 antagonists (ranitidine).
6. Parenteral steroids, typically methylprednisolone or
hydrocortisone, are recommended to dampen the late
allergic symptoms.
Treatment
84. Why are cancer pts at risk for life-
threatening infection?
• Chemotherapy
– Decreased number and
function of immune cells
• Radiation
• Surgeries
• Breakdown of
mucocutaneous barriers
• Foreign bodies (CVL,
grafts, etc.)
Meckler, Lindemulder. Emerg
Med Clin N Am, 2009.
86. Common Pathogens
GP
Bacteria
Staph spp
Strep spp
Enterococcus spp
Corynebacterium
spp
Bacillus spp
Clostridium spp
GN
Bacteria
E. Coli
Pseudomonas
aeruginosa
Klebsiella spp.
Enterobacter
Anaerobes
HSV, VZV
RSV, Influenza,
Parainfluenza
Adenovirus
Rotavirus,
enterovirus
CMV, EBV, HHV6
BK, JC
Candida spp
Aspergillus spp
Zygomycetes
Fusarium
Scedosporium
Cryptococcus
Viral Fungal Other
Pneumocystis
jiroveci
Protozoa
Meckler, Lindemulder. Emerg Med Clin N Am, 2009.
87. Risk group Assessment
High Risk
-Any malignancy
not controlled
-ANC <100/cumm
-Duration>7 days
-Toxic appearance
- Evidence of
infections.
Low risk
Dx: ALL, NHL in remission
ANC >100/cumm
Duration< 7 days
Non toxic appearance.
88. .
CBC with Differential
Blood culture from each CVC lumen
Culture from each suspicious lumen
Urine R/E, Culture
Stool R/E & culture
S. Electrolyte, S. Creatinine
CXR
For CNS symptoms CSF study &
CT Scan brain
Lab. Assessment
89. .
Supportive management
Empirical antibiotic therapy by broad spectrum with
antipseudomonal coverage
Monotherapy: cefepime, ceftazidime, imipenem,
meropenem, tazobactum/ piperacillin.
Dual Therapy: with monotherapy antibiotics Amikacin
or Gentamicin added.
Add gram positive coverage vancomycin and
clindamycin according to situation.
Change antibiotic according to culture report.
Empirical Antifungal
Management of Febrile Neutropenia
90. Shock
Common causes of shock in child with cancer
Management:
Ascertain cause and treat accordingly.
91. .
Also referred to as hepatic sinusoidal obstruction
syndrome.
Characterized by rapid and often massive hepatic
enlargement with resultant right-upper-quadrant pain,
liver tenderness, jaundice, weight gain, and ascites.
Ultrasonography shows ascites and reversal of flow in
hepatic vessels.
Etiology Preexisting hepatic disease, radiation,
allogeneic transplant, vincristine, actinomycin-D, and 6-
thiguanine, busulfan with or without
cyclophosphamide, and younger age.
Veno-Occlusive Disease
92. .
1. Primarily supportive in the nontransplant
setting including discontinuation of the
offending agent.
2. Studies evaluating defibrotide as a treatment
option are ongoing in the transplant setting.
Treatment
93. Summary
• Oncologic emergencies are common in the
pediatric population.
• The majority of these can be anticipated with
awareness of the clinical situation.
• Teamwork and communication among health
care professionals is essential for good
outcomes.
Editor's Notes
Urinary alkalinization increases uric acid solubility but decreases calcium phosphate solubility.
Alkalinization has
Unclear efficacy
Not routinely done anymore
Decreases Ca, P solubility