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 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.
Tumor lysis syndrome is characterized by metabolic imbalances that develop after chemotherapy treatment begins rapidly destroying cancer cells. It most often affects cancers with high proliferation rates and response to treatment, like aggressive lymphomas and leukemias. As malignant cells are destroyed, they release intracellular components into circulation, potentially causing hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. This can impair kidney function through uric acid crystallization in the renal tubules. Risk factors include high tumor burden, rapid growth rate, responsive cancer to therapy and preexisting hyperuricemia.
This document provides information about tumor lysis syndrome (TLS). TLS is an oncologic emergency caused by the rapid breakdown of tumor cells after initiation of chemotherapy. This releases intracellular contents like potassium, phosphate, and nucleic acids into circulation, which can overwhelm the kidneys and cause acute kidney injury. TLS risk is highest for certain cancers like acute lymphoblastic leukemia, non-Hodgkin's lymphoma, and acute myeloid leukemia. Prevention focuses on aggressive hydration and use of allopurinol or rasburicase to lower uric acid levels. Electrolyte abnormalities like hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia are managed to prevent complications like kidney damage. Early
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.
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 is an oncologic emergency caused by massive tumor cell lysis and release of potassium, phosphate, and nucleic acids into circulation. It often occurs after initiation of cytotoxic therapy in patients with high-grade lymphomas or ALL who have a large tumor burden or high proliferative rate. This can result in hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury due to uric acid precipitation in renal tubules. Aggressive hydration, allopurinol or rasburicase to reduce uric acid, phosphate binders, and renal replacement therapy if needed are used to treat and prevent tumor lysis syndrome.
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 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.
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.
Tumor lysis syndrome is characterized by metabolic imbalances that develop after chemotherapy treatment begins rapidly destroying cancer cells. It most often affects cancers with high proliferation rates and response to treatment, like aggressive lymphomas and leukemias. As malignant cells are destroyed, they release intracellular components into circulation, potentially causing hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. This can impair kidney function through uric acid crystallization in the renal tubules. Risk factors include high tumor burden, rapid growth rate, responsive cancer to therapy and preexisting hyperuricemia.
This document provides information about tumor lysis syndrome (TLS). TLS is an oncologic emergency caused by the rapid breakdown of tumor cells after initiation of chemotherapy. This releases intracellular contents like potassium, phosphate, and nucleic acids into circulation, which can overwhelm the kidneys and cause acute kidney injury. TLS risk is highest for certain cancers like acute lymphoblastic leukemia, non-Hodgkin's lymphoma, and acute myeloid leukemia. Prevention focuses on aggressive hydration and use of allopurinol or rasburicase to lower uric acid levels. Electrolyte abnormalities like hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia are managed to prevent complications like kidney damage. Early
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.
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 is an oncologic emergency caused by massive tumor cell lysis and release of potassium, phosphate, and nucleic acids into circulation. It often occurs after initiation of cytotoxic therapy in patients with high-grade lymphomas or ALL who have a large tumor burden or high proliferative rate. This can result in hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury due to uric acid precipitation in renal tubules. Aggressive hydration, allopurinol or rasburicase to reduce uric acid, phosphate binders, and renal replacement therapy if needed are used to treat and prevent tumor lysis syndrome.
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 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.
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.
RD, a 59-year-old male with newly diagnosed Burkitt's lymphoma, presents with high risk of tumor lysis syndrome based on his labs. The best treatment is rasburicase to rapidly reduce his high uric acid level and prevent renal failure, along with IV fluids and allopurinol for comprehensive management.
MM, a 62-year-old female with severe febrile neutropenia following chemotherapy, requires inpatient treatment with broad-spectrum IV antibiotics like meropenem and vancomycin due to her high risk status from low ANC, mucositis, and hypotension.
This document provides guidelines for prevention, risk stratification, and treatment of tumor lysis syndrome
Tumor lysis syndrome and hypercalcemia of malignancyGaurav Kumar
This document discusses hypercalcemia and tumor lysis syndrome. It defines hypercalcemia as calcium levels above normal physiological range. The main causes of hypercalcemia include parathyroid disorders, malignancy, vitamin D abnormalities, and renal failure. Symptoms range from mild to severe depending on calcium level. Tumor lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing electrolytes. This can cause hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, potentially leading to renal failure. The document outlines evaluation, treatment and prevention of both conditions.
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.
A 35-year-old man presented with increasing headaches, palpitations, anxiety, and panic attacks over the past six months. His history and examination were consistent with possible conditions including anxiety disorders, hyperthyroidism, and pheochromocytoma. Pheochromocytoma was considered the most likely diagnosis given the classic signs and symptoms. Pheochromocytomas are rare catecholamine-secreting tumors that typically arise from the adrenal medulla or sympathetic ganglia. Diagnostic testing revealed elevated levels of catecholamines and metanephrines confirming the diagnosis of a pheochromocytoma. The patient was started on alpha- and beta-blockers in preparation for surgical removal of the tumor.
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 discusses malignant hypercalcaemia, which occurs in 10% of cancer patients and is caused by bone metastases or humoral factors released by tumour cells. It leads to high calcium levels in the blood (>3.0 mmol/L) and poor prognosis, with most patients dying within a year. The document outlines the physiology and clinical manifestations of hypercalcaemia and provides recommendations for investigations and management, including rehydration, calcium restriction, bisphosphonates, calcitonin, and targeting the underlying malignancy.
Hypokalemia is defined as a serum potassium level lower than 3.5 mEq/L. It is usually asymptomatic when mild but can cause muscle weakness, cardiac arrhythmias, and paralysis in more severe cases. Causes include drugs, diet, diarrhea, vomiting, hyperthyroidism, and Cushing's syndrome. Diagnosis involves medical history, physical exam, electrolyte tests, ECG, and investigating the underlying cause. Treatment focuses on replacing potassium deficits orally or intravenously while addressing the underlying condition.
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 discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
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
This document discusses malignant spinal cord compression, its causes, symptoms, diagnosis and treatment. It begins by differentiating between extramedullary vs intradural vs intramedullary compression. Common symptoms include pain, motor deficits, sensory changes and autonomic dysfunction. Metastatic tumors are the most frequent cause. Diagnosis involves imaging like MRI, CT and bone scans. Treatment aims to relieve pain and prevent further cord compression, and may involve surgery, radiation or supportive care depending on the extent of disease and patient prognosis. Early detection and treatment can help preserve neurological function.
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
This document discusses the management of urinary calculus (kidney stones). It covers the anatomy, epidemiology, risk factors, types, pathophysiology, clinical presentations, investigations, and treatment options. Treatment depends on factors like the stone size and location, availability of treatment modalities, and patient anatomy. Options include conservative management, surgery like ureteroscopy, percutaneous nephrolithotomy (PCNL), and extracorporeal shockwave lithotripsy (ESWL).
Hepatoblastoma- Investigations and managementARJUN MANDADE
This document summarizes information about hepatoblastoma, a rare type of liver cancer that mostly affects young children. It discusses the history and terminology of hepatoblastoma. Key points include: hepatoblastoma typically affects children under 3 years old and accounts for about 1% of childhood cancers. Complete surgical resection is the main treatment when possible but less than 50% of patients are resectable at diagnosis. The addition of cisplatin-based chemotherapy has improved outcomes by increasing resectability. Prognosis remains suboptimal for patients with unresectable or metastatic disease after chemotherapy. Chemoembolization and liver transplantation are promising alternative treatments in these cases.
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.
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.
Carcinoma of the prostate is the most commonly diagnosed cancer and second leading cause of cancer death in men. Risk increases with age and family history. It often metastasizes to bones and lymph nodes. Diagnosis involves elevated PSA levels, abnormal digital rectal exam, biopsy. Staging uses the TNM system - early stages are limited to the prostate while advanced stages have spread outside the prostate. Gleason scoring evaluates microscopic patterns to determine tumor grade and aggressiveness. Treatment depends on tumor stage, grade and patient health.
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
This document discusses urinary stone disease (kidney stones). It reviews the epidemiology, risk factors, pathogenesis and types of kidney stones. It also reviews guidelines for management from the American Urological Association. The main points are:
- Kidney stone prevalence is increasing worldwide, especially for calcium stones. Risk factors include metabolic syndrome, obesity, diabetes and cardiovascular disease.
- The major stone types are calcium oxalate, calcium phosphate, uric acid and struvite. Composition depends on urine composition and risk factors.
- Pathogenesis involves supersaturation of urine leading to crystallization of stone-forming substances. Hypocitraturia and hyperoxaluria are common contributing factors.
-
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.
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.
RD, a 59-year-old male with newly diagnosed Burkitt's lymphoma, presents with high risk of tumor lysis syndrome based on his labs. The best treatment is rasburicase to rapidly reduce his high uric acid level and prevent renal failure, along with IV fluids and allopurinol for comprehensive management.
MM, a 62-year-old female with severe febrile neutropenia following chemotherapy, requires inpatient treatment with broad-spectrum IV antibiotics like meropenem and vancomycin due to her high risk status from low ANC, mucositis, and hypotension.
This document provides guidelines for prevention, risk stratification, and treatment of tumor lysis syndrome
Tumor lysis syndrome and hypercalcemia of malignancyGaurav Kumar
This document discusses hypercalcemia and tumor lysis syndrome. It defines hypercalcemia as calcium levels above normal physiological range. The main causes of hypercalcemia include parathyroid disorders, malignancy, vitamin D abnormalities, and renal failure. Symptoms range from mild to severe depending on calcium level. Tumor lysis syndrome occurs when large numbers of cancer cells break down rapidly, releasing electrolytes. This can cause hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia, potentially leading to renal failure. The document outlines evaluation, treatment and prevention of both conditions.
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.
A 35-year-old man presented with increasing headaches, palpitations, anxiety, and panic attacks over the past six months. His history and examination were consistent with possible conditions including anxiety disorders, hyperthyroidism, and pheochromocytoma. Pheochromocytoma was considered the most likely diagnosis given the classic signs and symptoms. Pheochromocytomas are rare catecholamine-secreting tumors that typically arise from the adrenal medulla or sympathetic ganglia. Diagnostic testing revealed elevated levels of catecholamines and metanephrines confirming the diagnosis of a pheochromocytoma. The patient was started on alpha- and beta-blockers in preparation for surgical removal of the tumor.
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 discusses malignant hypercalcaemia, which occurs in 10% of cancer patients and is caused by bone metastases or humoral factors released by tumour cells. It leads to high calcium levels in the blood (>3.0 mmol/L) and poor prognosis, with most patients dying within a year. The document outlines the physiology and clinical manifestations of hypercalcaemia and provides recommendations for investigations and management, including rehydration, calcium restriction, bisphosphonates, calcitonin, and targeting the underlying malignancy.
Hypokalemia is defined as a serum potassium level lower than 3.5 mEq/L. It is usually asymptomatic when mild but can cause muscle weakness, cardiac arrhythmias, and paralysis in more severe cases. Causes include drugs, diet, diarrhea, vomiting, hyperthyroidism, and Cushing's syndrome. Diagnosis involves medical history, physical exam, electrolyte tests, ECG, and investigating the underlying cause. Treatment focuses on replacing potassium deficits orally or intravenously while addressing the underlying condition.
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 discusses the case of a 56-year-old woman who presented with fever, sore throat, and breathlessness and was diagnosed with thyroid storm. It provides details on her medical history, examination, labs, and treatment. The document also discusses two additional cases of thyroid storm and provides a summary of key points on diagnosing and treating thyroid storm.
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
This document discusses malignant spinal cord compression, its causes, symptoms, diagnosis and treatment. It begins by differentiating between extramedullary vs intradural vs intramedullary compression. Common symptoms include pain, motor deficits, sensory changes and autonomic dysfunction. Metastatic tumors are the most frequent cause. Diagnosis involves imaging like MRI, CT and bone scans. Treatment aims to relieve pain and prevent further cord compression, and may involve surgery, radiation or supportive care depending on the extent of disease and patient prognosis. Early detection and treatment can help preserve neurological function.
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
This document discusses the management of urinary calculus (kidney stones). It covers the anatomy, epidemiology, risk factors, types, pathophysiology, clinical presentations, investigations, and treatment options. Treatment depends on factors like the stone size and location, availability of treatment modalities, and patient anatomy. Options include conservative management, surgery like ureteroscopy, percutaneous nephrolithotomy (PCNL), and extracorporeal shockwave lithotripsy (ESWL).
Hepatoblastoma- Investigations and managementARJUN MANDADE
This document summarizes information about hepatoblastoma, a rare type of liver cancer that mostly affects young children. It discusses the history and terminology of hepatoblastoma. Key points include: hepatoblastoma typically affects children under 3 years old and accounts for about 1% of childhood cancers. Complete surgical resection is the main treatment when possible but less than 50% of patients are resectable at diagnosis. The addition of cisplatin-based chemotherapy has improved outcomes by increasing resectability. Prognosis remains suboptimal for patients with unresectable or metastatic disease after chemotherapy. Chemoembolization and liver transplantation are promising alternative treatments in these cases.
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.
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.
Carcinoma of the prostate is the most commonly diagnosed cancer and second leading cause of cancer death in men. Risk increases with age and family history. It often metastasizes to bones and lymph nodes. Diagnosis involves elevated PSA levels, abnormal digital rectal exam, biopsy. Staging uses the TNM system - early stages are limited to the prostate while advanced stages have spread outside the prostate. Gleason scoring evaluates microscopic patterns to determine tumor grade and aggressiveness. Treatment depends on tumor stage, grade and patient health.
Hyperkalemia is defined as a plasma potassium level above 5.5 mEq/L. It can be caused by a shift of potassium from intracellular to extracellular space due to acidosis or tissue damage. Other causes include reduced renal excretion due to medications like ACE inhibitors or renal failure. Symptoms range from none to muscle weakness to cardiac arrhythmias. Treatment involves calcium to antagonize cardiac effects, insulin or beta-agonists to shift potassium intracellularly, and cation exchange resins or dialysis to remove excess potassium.
This document discusses urinary stone disease (kidney stones). It reviews the epidemiology, risk factors, pathogenesis and types of kidney stones. It also reviews guidelines for management from the American Urological Association. The main points are:
- Kidney stone prevalence is increasing worldwide, especially for calcium stones. Risk factors include metabolic syndrome, obesity, diabetes and cardiovascular disease.
- The major stone types are calcium oxalate, calcium phosphate, uric acid and struvite. Composition depends on urine composition and risk factors.
- Pathogenesis involves supersaturation of urine leading to crystallization of stone-forming substances. Hypocitraturia and hyperoxaluria are common contributing factors.
-
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 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 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.
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
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.
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.
Hepatocellular carcinoma (HCC) is the most common type of liver cancer. It has a high worldwide incidence, especially in areas where hepatitis B is prevalent like Southeast Asia. Major risk factors for HCC include hepatitis B and C infections, cirrhosis of the liver from any cause, and alcohol abuse. The disease progresses as hepatocytes undergo repeated cycles of cell death and regeneration due to chronic inflammation and cirrhosis, accumulating mutations over time that can lead to cancer. Diagnosis involves blood tests, imaging like ultrasound or CT scan, and often a biopsy. Staging systems evaluate tumor characteristics, liver function, and physical status to determine prognosis and treatment options. Treatment may include surgical resection, liver transplantation, ablation
This document outlines several oncological emergencies including tumor lysis syndrome, hyperleukocytosis, disseminated intravascular coagulopathy, superior vena cava obstruction, febrile neutropenia, and infection. It provides details on the characteristics, risks factors, signs and symptoms, and management approaches for each emergency. Key aspects of management include hydration, monitoring of electrolytes and blood counts, use of allopurinol or steroids to prevent tumor lysis, platelet transfusions for coagulopathies, and early treatment of febrile neutropenia with antibiotics. The document emphasizes the need for prompt recognition and treatment of these potentially life-threatening oncological complications.
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.
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3. KEY POINTS
•
Tumor lysis syndrome (TLS) is a metabolic derangement resulting from massive
destruction of malignant cells, leading to electrolyte abnormalities and, consequently,
renal, cardiac, and neurologic dysfunction and possibly death if left untreated
•
Symptoms of TLS can occur spontaneously but usually occur within 12 to 72 hours after
initiation of cytoreductive chemotherapy in patients with hematologic malignancies or high
tumor burden
•
Treatment consists of intravenous hydration and potassium-, phosphate-, and/or uric acidlowering medications or dialysis when indicated
•
Complications, such as acute renal failure, electrolyte disturbances, seizures, and
arrhythmias, can compromise further cancer therapy or lead to death
•
Early identification and prophylactic management of patients at risk for TLS may prevent
potentially life-threatening sequelae
4. BACKGROUND - DESCRIPTION
•
TLS is caused by the massive and abrupt release of cellular components, including
nucleic acids, potassium, and phosphates, from malignant cells into the blood, which
usually occurs with the initiation of cytotoxic therapy but, rarely, can occur spontaneously
•
Hyperuricemia, lactic acidosis, hyperphosphatemia, hyperkalemia, and secondary
hypocalcemia occur as a result of TLS
•
Hyperuricemia is defined as a plasma or serum uric acid concentration greater than the
upper limit of normal (usually >7.4 mg/dL in male patients and >5.8 mg/dL in female
patients)
•
TLS occurring during induction chemotherapy that is characterized by laboratory
abnormalities traditionally is classified as laboratory TLS, whereas clinical TLS includes
both laboratory abnormalities and clinical features.
•
Only a minority of patients with laboratory TLS will develop clinical TLS
5. BACKGROUND - EPIDEMIOLOGY
•
The incidence of TLS differs according to the type of tumor and the definition of TLS
•
A population-based study in patients with acute myeloid leukemia undergoing induction
chemotherapy found that 12% of patients had laboratory TLS, and 5% had clinical TLS.
Only clinical TLS was associated with a higher mortality rate
•
A retrospective study in patients with intermediate- to high-grade non-Hodgkin lymphoma
found that the incidence of laboratory TLS was 42%, and the incidence of clinical TLS was
approximately 6%
6. CAUSES & RISK FACTORS - CAUSES
•
TLS is caused by the sudden destruction of a large number of malignant cells, resulting in
the massive release of intracellular nucleic acids (metabolized to uric acid), potassium,
and phosphorus into the blood
7. CAUSES & RISK FACTORS - RISK FACTORS
•
Tumor grade, tumor burden, and degree of chemosensitivity: TLS is more likely to occur
in patients with high-grade tumors with a large burden and high chemosensitivity, such as
hematologic malignancies, small-cell cancer, and germ cell tumors, and is associated less
commonly with chemo-insensitive tumors, such as melanoma, and hepatocellular
carcinoma
•
Type of therapy: TLS is more likely to occur with chemotherapy and is associated less
commonly with targeted therapies and radiation therapy; however, the condition also may
occur spontaneously before treatment
•
Patient-related factors include the following:
• Compromised kidney function due to preexisting renal dysfunction or dehydration,
concurrent use of nephrotoxic drugs, or renal obstruction
• Preexisting hyperuricemia from any cause
• Systemic infection
9. PRIMARY PREVENTION
•
Prevention of TLS focuses on monitoring fluid intake and output and uric acid, electrolyte
(serum phosphorus, potassium, and calcium), creatinine, and lactate dehydrogenase
(LDH) levels before and during cytotoxic therapy
•
The frequency of monitoring depends on the risk of developing clinical TLS
•
Laboratory testing should be done daily in low-risk patients, every 8 to 12 hours in
intermediate-risk patients, and every 6 to 8 hours in high-risk patients
10. POPULATION AT RISK
•
Patients with lymphomas (e.g., non-Hodgkin lymphomas, including Burkitt lymphoma,
lymphoblastic lymphoma, and diffuse large-cell lymphoma), leukemias (e.g., acute
lymphoblastic leukemia, acute myelogenous leukemia), or solid tumors with high
proliferative rates (e.g., small-cell lung cancer and germ cell tumors)
•
Patients with increased tumor burden as evidenced by bulky disease, baseline elevated
LDH levels, and hyperleukocytosis
•
Patients with preexisting renal failure
•
Patients with baseline elevated uric acid levels
11. POPULATION AT RISK
•
In 2010, an international TLS expert consensus panel published comprehensive guidelines for assessing the
risk of TLS, which incorporated renal function status as well as cancer types. The risk of developing TLS
was divided into three categories:
•
•
Intermediate risk (1%-5% risk of developing TLS), such as in patients with abnormal kidney function
and/or renal involvement and low-risk diseases; adults with non-bulky, diffuse, large B-cell
lymphoma and elevated LDH levels; patients with early-stage aggressive lymphomas and LDH
levels greater than twice the upper normal limit; patients with acute myelogenous leukemia and a
leukocyte count of 25,000 to 100,000/µL; and patients with acute lymphoblastic leukemia, an LDH
level less than twice the upper normal limit, and a leukocyte count <100,000/µL
•
•
Low risk (less than 1% risk of developing TLS), such as in patients with normal kidney function/no
renal involvement and Hodgkin lymphoma, indolent lymphomas, or solid tumors
High risk (greater than 5% risk of developing TLS), such as in adults with bulky, diffuse, large Bcell lymphoma and elevated LDH levels; patients with advanced-stage aggressive lymphomas (eg,
Burkitt lymphoma/leukemia); patients with intermediate-risk disease and abnormal kidney function
and/or renal involvement; and patients with acute leukemias (myeloid and lymphoid) and a leukocyte
count >100,000/µL
Intravenous hydration and anti-hyperuricemic therapy also should be considered
12. PREVENTIVE MEASURES
•
Patients at risk of developing TLS should be monitored closely, especially in the first 72
hours of treatment. Serum electrolyte, LDH, and uric acid levels should be measured
frequently, depending on the risk of developing TLS
•
Use of nephrotoxic agents, including contrast dye, should be avoided in patients with
underlying renal dysfunction who are scheduled to undergo induction chemotherapy
•
Use of loop diuretics is controversial in light of studies showing that diuretics do not
decrease mortality and morbidity and should only be considered in adults without
hypovolemia or obstructive uropathy in order to maintain urine output >100 mL/hr
•
Urine alkalinization with sodium bicarbonate has been found to be ineffective in
preventing uric acid nephropathy and has been associated with increased precipitation of
calcium phosphate and xanthine in the renal tubules and, therefore, is no longer
recommended, except in special situations, such as in patients with metabolic acidosis
• Alkalinization of the urine is not necessary in patients receiving treatment with
rasburicase
13. PREVENTIVE MEASURES
•
Aggressive intravenous hydration (normal saline, 2 to 3 L/m2/d in adults) is the primary
preventive strategy for TLS and is most effective if initiated 48 hours before and continued
for 72 hours after cytotoxic therapy
•
The goal is to enhance urine flow (urine output of 80-100 mL/m2/h), promote the excretion
of uric acid and phosphorus, and decrease the risk of uric acid precipitation in the renal
tubules
•
Caution must be exercised in elderly patients and in patients with compromised cardiac
function due to the risk of fluid overload
14. PREVENTIVE MEASURES
•
Anti-hyperuricemic therapy should be considered in patients with a 1% or higher risk of
developing TLS
•
The choice of agent depends on the degree of risk and lack of contraindications
•
Allopurinol, a xanthine oxidase inhibitor, is recommended in patients with a 5% or lower
risk of developing TLS and in patients with a greater than 5% risk in whom rasburicase is
contraindicated. Several studies have shown allopurinol to be effective in improving uric
acid levels in patients with preexisting hyperuricemia and in preventing uric acid elevation
in patients with normal pretreatment uric acid levels
•
Rasburicase, a recombinant urate oxidase, is the agent of choice in patients with a
greater than 5% risk of developing TLS, no history of hypersensitivity or hematologic
reactions to rasburicase, and without glucose-6-phosphatase dehydrogenase (G6PD)
deficiency. Several drug trials and a systematic review in pediatric patients have shown
rasburicase to be effective in preventing and reversing TLS-associated hyperuricemia in
both children and adults
15. PREVENTIVE MEASURES
•
The diagnosis of TLS should be considered in any patient with risk factors for TLS in whom chemotherapy
has been initiated
•
The symptoms and signs of TLS are usually nonspecific. Laboratory values are critical for diagnosis
•
Laboratory TLS was defined as the presence of two or more of the following criteria within 3 days before
or 7 days after the initiation of chemotherapy:
•
•
Potassium level =6.0 mEq/L or a 25% increase from baseline
•
Phosphorus level =6.5 mg/dL or a 25% increase from baseline
•
•
Uric acid level =8 mg/dL or a 25% increase from baseline
Calcium level =7 mg/dL or a 25% decrease from baseline
Clinical TLS was defined as the presence of laboratory TLS and one or more of the following criteria:
•
Creatinine level =1.5 times the upper limit of normal
•
Cardiac arrhythmia or sudden death due to hyperkalemia
•
Seizure
16. CLINICAL PRESENTATION - SYMPTOMS
•
Patients may be asymptomatic
•
When present, symptoms are nonspecific and usually reflect the associated metabolic
abnormalities (uremia, hyperkalemia, hyperphosphatemia, and hypocalcemia) directly or
indirectly, with abnormal renal, cardiac, and/or neurologic function, such as:
• Palpitations with associated dyspnea, dizziness, and syncope
• Symptoms of heart failure, such as swelling and orthopnea
• Anorexia, nausea, vomiting, and diarrhea
• Oliguria and hematuria
• Lethargy
• Signs
17. CLINICAL PRESENTATION - SIGNS
•
When present, signs are nonspecific and usually reflect the associated metabolic
abnormalities (uremia, hyperkalemia, hyperphosphatemia, and hypocalcemia) directly or
indirectly, with abnormal renal, cardiac, and/or neurologic function, such as:
• Tachycardia or bradycardia, hypotension, and decreased urine output
• Irregular heart rate due to arrhythmias
• Chvostek sign may be elicited in patients with hypocalcemia
• Jugular venous distension and dependent edema if heart failure is present
• Altered mental status and disorientation related to electrolyte disturbances or
postictal state
• Evidence of seizures, such as tongue biting, incontinence, or bodily injury
• Sudden death
18. DIAGNOSTIC TESTING
•
Measurement of the following is indicated:
• Serum uric acid, as elevated levels can represent either preexisting hyperuricemia
and/or one component of TLS
• Serum potassium, as elevated levels are seen characteristically before the maximal
levels of phosphorus and uric acid are reached and can potentiate arrhythmias
• Serum phosphorus, as abnormal levels can lead to secondary hypocalcemia
•
Renal function tests may show impaired renal function secondary to deposition of uric
acid and calcium phosphate in renal tubules
•
Electrocardiographic findings are reflective of electrolyte abnormalities
19. DIFFERENTIAL DIAGNOSIS
•
Hyperuricemia without other features of TLS can be caused by uric acid overproduction
and/or decreased excretion. Patients may have a previous history of hyperuricemia.
• Quantification of uric acid excretion can aid in establishing the diagnosis
•
Overproduction and decreased excretion of uric acid are seen in patients with idiopathic
primary hyperuricemia or gout (acute or chronic)
•
Overproduction of uric acid is seen in the setting of certain malignancies, such as
myeloproliferative disorders (e.g., polycythemia vera), leukemias, lymphomas, plasma cell
disorders, and small-cell lung cancer; chemotherapy for malignancy; congenital
syndromes; psoriasis; obesity; and alcohol abuse
•
Decreased excretion of uric acid is seen in patients with reduced renal function,
congenital syndromes, hyperparathyroidism, or hypothyroidism and may occur as a result
of treatment with medications such as diuretics, nicotinic acid, salicylates, and
cyclosporine
20. DIFFERENTIAL DIAGNOSIS
•
TLS must be differentiated from other causes of electrolyte disturbances and renal
dysfunction that may occur in patients with cancer and that may require specific
treatment, such as renal failure
•
Patients with cancer are at increased risk for renal dysfunction due to volume depletion,
obstructive uropathy, and acute tubular necrosis from nephrotoxic drugs used in treatment
(e.g., antibiotics, contrast dye, and chemotherapeutic agents)
•
A thorough history and physical examination, urinalysis and microscopy, and
ultrasonography may aid in differentiation
•
Hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia may be associated
with acute renal failure regardless of the underlying etiology
•
In patients with TLS, the rapid lysis of malignant cells causes hyperuricemia, lactic
acidosis, hyperphosphatemia, hyperkalemia, and secondary hypocalcemia and may
progress to acute renal failure in a minority of patients
21. CONSULTATION
•
Consultation with a nephrologist should be considered for assistance in diagnosing renal
dysfunction
•
A hematologist/oncologist should be consulted for treatment of any underlying malignancy
22. TREATMENT - SUMMARY
•
TLS is a life-threatening condition that necessitates immediate action and close
monitoring
•
Clinical TLS can develop despite appropriate preventive measures
•
The primary goal of treatment is correction of electrolyte disturbances
•
Medications and other agents (e.g., radiocontrast dye) that may exacerbate kidney injury
should be avoided
•
Dialysis is recommended in patients with refractory hyperkalemia, acidosis, fluid overload,
uric acid levels >15 mg/dL, or uremic symptoms
23. TREATMENT - SUMMARY
•
In patients with hyperkalemia:
• Intravenous or oral potassium should be avoided, and potassium-lowering
medications, such as sodium polystyrene sulfonate, should be considered
•
In patients with symptomatic or severe hyperkalemia:
• Calcium gluconate should be administered to decrease myocardial membrane
excitability
•
Emergency treatment to shift potassium intracellularly includes one or more of the
following: regular insulin and dextrose, nebulized albuterol, and sodium bicarbonate
•
Therapies to decrease the total body potassium content include sodium polystyrene
sulfonate and hemodialysis or peritoneal dialysis
24. TREATMENT - SUMMARY
•
In patients with hyperphosphatemia:
• Phosphorus intake should be minimized
• Calcium salts should not be administered, unless the patient has severe symptoms
due to hypocalcemia or severe and/or symptomatic hyperkalemia. Otherwise,
calcium salts may cause calcium phosphate precipitation
• Preferred phosphate binders include aluminum hydroxide, sevelamer hydrochloride,
and lanthanum carbonate
•
Hemodialysis is indicated if there is no response to medical therapy
25. TREATMENT - SUMMARY
•
In patients with symptomatic hypocalcemia, slow administration of calcium gluconate (50100 mg/kg/dose intravenously) should be considered; close monitoring is necessary due
to the potentially increased risk of calcium phosphate deposition
•
In adult patients with hyperuricemia, treatment with allopurinol or rasburicase is indicated
26. CONTRAINDICATIONS TO
ALLOPURINOL OR RASBURICASE
•
Both agents should be avoided in patients with hypersensitivity to the drug or any other
component.
•
Rasburicase is contraindicated in patients with G6PD deficiency
29. SPECIAL CIRCUMSTANCES - COMORBIDITIES
•
Patients with preexisting renal failure or hyperuricemia are at increased risk of developing
TLS, and management of fluid and electrolyte status is more challenging
•
Patients taking allopurinol or urosuric agents for coexisting gout or chronic hyperuricemia
may have a decreased risk of TLS; if TLS does occur, the rapid increase in serum uric
acid levels may precipitate a gouty attack
•
Patient satisfaction/lifestyle priorities
•
TLS is associated with increased morbidity and mortality, as it may delay future
administration of chemotherapy and other cancer therapies, may lead to renal failure
requiring dialysis, and is associated with the possibility of fatal arrhythmias
30. FOLLOW-UP - MONITORING
•
Fluid intake and output, cardiac status, uric acid levels, electrolyte (serum phosphorus,
potassium, and calcium) levels, creatinine levels, and LDH levels should be monitored
every 4 to 6 hours in patients with clinical TLS and every 6 to 8 hours in patients with
laboratory TLS
•
According to the 2008 American Society of Clinical Oncology guidelines, uric acid levels
should be reevaluated 4 hours after administration of rasburicase and every 6 to 8 hours
thereafter until resolution of TLS
31. PROGNOSIS
•
In patients with acute myelogenous leukemia, the development of clinical TLS was
associated with a 2% mortality rate from induction therapy
•
Patients with acute TLS and acute kidney injury have an increased mortality rate (both in
hospital and at 6 months) compared to patients without renal injury
32. COMPLICATIONS
•
Complications associated with TLS:
• Acute renal failure
• Elevated serum phosphate levels can lead to secondary hypocalcemia due to
calcium phosphate crystal formation, resulting in tissue calcification and
nephrocalcinosis
• Hyperkalemia can lead to potentially fatal arrhythmias
•
Complications associated with therapy:
• Hydration may lead to volume overload and congestive heart failure in patients with
compromised cardiac function
• Allopurinol may cause severe hypersensitivity reactions
• Rasburicase may cause hemolysis in patients with G6PD deficiency
33. PATIENT EDUCATION
•
Patients should be informed of the following:
• TLS primarily is encountered at the time of initiation of chemotherapy but may occur
before starting any therapy
• The syndrome results from the release of the contents of cancer cells after being
killed by chemotherapy and can be life-threatening, potentially leading to kidney
failure and/or death
• The best approach to prevention is administration of fluids and agents that affect the
formation or metabolism of uric acid
34. QUESTION
A patient with extremely severe myeloma with a plasmacytoma is admitted for combination
chemotherapy. Two days later, the creatinine rises. What is the most likely cause?
•
A. Cisplatin
•
B. Hyperuricemia
•
C. Bence-Jones proteinuria
•
D. Hypercalcemia
•
E. Hyperoxaluria
B. Two days after chemotherapy, the creatinine rises in a person with a hematologic malignancy.
This is most likely from tumor lysis syndrome leading to hyperuricemia. Cisplatin, as with most drug
toxicities, would not produce a rise in creatinine for 5 to 10 days. Bence-Jones protein and
hypercalcemia both cause renal insufficiency, but it would not be rapid and it would not happen as a
result of treatment. Treatment for myeloma would end up decreasing both the calcium and BenceJones protein levels because they are produced from the leukemic cells. Cancer cells do not
release oxalate.
35. ADDITIONAL QUESTION
What would have prevented this event?
•
Allopurinol, hydration, and rasburicase should have been given prior to chemotherapy to
prevent renal failure from tumor lysis syndrome
36. NOW, WHAT DID YOU LEARN?
What are the main risk factors associated with TLS?
•
TLS is more likely to develop in patients with a high tumor burden, a tumor that is sensitive to
cytotoxic therapies, or preexisting renal disease. TLS occurs most commonly during induction
chemotherapy in patients with hematologic malignancies
What additional criteria are needed for laboratory TLS to be considered clinical TLS?
•
Clinical TLS is defined as laboratory TLS in addition to a creatinine level =1.5 times the upper
limit of normal, cardiac arrhythmia or sudden death, or seizure
What is the approach to prevention of TLS?
•
There are two main components: maintenance of urine output through hydration and use of
antihyperuricemic agents. Hydration and treatment with allopurinol should be started 48 hours
before and continued for 72 hours after initiation of cytotoxic therapy.
•
Treatment with rasburicase can be started earlier, as efficacy is seen within 4 hours, thereby
allowing chemotherapy to be initiated earlier
37. NOW, WHAT DID YOU LEARN?
How is TLS treated?
•
Treatment consists of aggressive supportive care, correction of any electrolyte
disturbances, and administration of allopurinol or rasburicase
What are the main contraindications to treatment with allopurinol or rasburicase?
•
Both agents should be avoided in patients with hypersensitivity to the drug or any other
component
•
Rasburicase is contraindicated in patients with G6PD deficiency
38. REFERENCES
•
1) Smalley RV, Guaspari A, Haase-Statz S, Anderson SA, Cederberg D, Hohneker JA. Allopurinol:
intravenous use for prevention and treatment of hyperuricemia. J Clin Oncol. 2000;18:1758-63
•
2) Cheuk DK, Chiang AK, Chan GC, Ha SY. Urate oxidase for the prevention and treatment of
tumor lysis syndrome in children with cancer. Cochrane Database Syst Rev. 2010:CD006945
•
3) Coiffier B, Mounier N, Bologna S, et al. Efficacy and safety of rasburicase (recombinant urate
oxidase) for the prevention and treatment of hyperuricemia during induction chemotherapy of
aggressive non-Hodgkin's lymphoma: results of the GRAAL1 (Groupe d'Etude des Lymphomes
de l'Adulte Trial on Rasburicase Activity in Adult Lymphoma) study. J Clin Oncol. 2003;21:4402-6
•
4) Cortes J, Moore JO, Maziarz RT, et al. Control of plasma uric acid in adults at risk for tumor
Lysis syndrome: efficacy and safety of rasburicase alone and rasburicase followed by allopurinol
compared with allopurinol alone—results of a multicenter phase III study. J Clin Oncol.
2010;28:4207-13
•
5) Jeha S, Kantarjian H, Irwin D, et al. Efficacy and safety of rasburicase, a recombinant urate
oxidase (Elitek), in the management of malignancy-associated hyperuricemia in pediatric and
adult patients: final results of a multicenter compassionate use trial. Leukemia. 2005;19:34-8
EvidenceAllopurinol: A multicenter, retrospective review collected data over a 21-year period on 1,172 adults and children with restricted oral intake who received intravenous allopurinol as an adjunct to chemotherapy based on compassionate plea. Serum uric acid levels normalized or improved in 87% of adults and 95% of children. When administered prophylactically in patients at high risk of developing TLS, intravenous allopurinol prevented an increase in uric acid levels in 93% of adults and 92% of children.[1]Level of evidence: 3Rasburicase: A systematic review of five trials evaluating the efficacy and safety of urate oxidase for prevention and treatment of TLS in a total of 794 pediatric patients found that although frequency of normalization of uric acid levels was significantly improved in the treatment groups (relative risk, 19.09 [95% confidence interval, 1.28-285.41]), there was no difference in overall mortality or incidence of renal failure.[2]Level of evidence: 1A phase II, single-arm, open-label study evaluated the benefit of rasburicase in 100 adults with aggressive non-Hodgkin lymphoma who were at risk for hyperuricemia during the first cycle of chemotherapy, 66% of whom had elevated LDH levels and 11% of whom had hyperuricemia (uric acid level >7.56 mg/dL) before chemotherapy. All patients had a good response to rasburicase, with normalization of uric acid levels within 4 hours.[3]Level of evidence: 3A phase III study compared the efficacy of rasburicase, 0.20 mg/kg/d intravenously on days 1 to 5, versus rasburicase, 0.20 mg/kg/d intravenously on days 1 to 3, plus allopurinol, 300 mg/d orally on days 3 to 5, versus allopurinol, 300 mg/d orally on days 1 to 5, for control of serum uric acid levels in 275 adults with hematologic malignancies who were at risk for hyperuricemia and TLS. Plasma uric acid levels were reduced or maintained at =7.5 mg/dL in 87% of patients receiving rasburicase alone, 78% of patients receiving rasburicase followed by allopurinol, and 66% of patients receiving allopurinol alone. Rasburicase was significantly superior to allopurinol (P = .001), and there were no significant differences in the incidence or severity of adverse events.[4]Level of evidence: 3A multicenter compassionate use trial in 1,069 patients (682 children and 387 adults) with cancer presenting with or at risk for acute hyperuricemia and TLS found that administration of rasburicase, 0.20 mg/kg intravenously for 1 to 7 days, reduced uric acid levels to normal in all patients.[5]Level of evidence: 3