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 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 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 (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.
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
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 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 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.
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 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 (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.
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
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 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 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.
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.
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.
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.
Heart failure and liver dysfunction By Dr. Vaibhav Yawalkar MD,DM Cardiologyvaibhavyawalkar
1) Heart failure and liver disease often coexist due to shared risk factors and pathophysiological mechanisms that affect both organs.
2) Impaired cardiac function can lead to hepatic dysfunction through liver hypoperfusion and congestion, while liver disease can also cause cardiomyopathy.
3) Understanding the cardio-hepatic interactions and exploring therapeutic targets like liver X receptors and the gut microbiome may help manage patients with both heart failure and liver disease.
Tumour lysis syndrome (TLS) is a metabolic condition caused by the breakdown of malignant cells, characterized by electrolyte abnormalities like hyperuricaemia, hyperphosphataemia, hyperkalaemia and hypocalcaemia. It can occur before, during or after treatment for malignancy. Clinical TLS involves organ failure from electrolyte imbalances. Risk factors include extensive tumour burden and poor renal function. Prevention involves monitoring for symptoms and electrolyte levels before and after therapy. Treatment focuses on correcting electrolyte abnormalities through hydration, diuretics, binders, insulin therapy and dialysis if needed.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves systemic conditions affecting both organs. Early diagnosis and treatment tailored to the CRS subtype is important for improving outcomes.
This document discusses thrombocytopenia, providing information on:
- Causes including decreased platelet production, sequestration, and increased destruction.
- Idiopathic thrombocytopenic purpura (ITP), the most common cause in children, which is an autoimmune condition where antibodies destroy platelets.
- Clinical presentation, diagnosis, treatment including corticosteroids, IVIG, and splenectomy for severe or chronic cases.
- Other considerations like drug-induced thrombocytopenia and conditions involving nonimmune platelet destruction.
This document discusses Heparin-Induced Thrombocytopenia (HIT). It covers the immunology of HIT including how antibodies form against platelet factor 4. It describes the clinical presentations of HIT focusing on the 4Ts criteria of thrombocytopenia, timing of platelet drop, thrombosis, and other causes. It discusses laboratory diagnosis using assays to detect antibodies. The document concludes with sections on treatment options including alternative anticoagulants and managing HIT in different clinical scenarios.
1) The patient's platelet count decreased while receiving heparin therapy, with counts dropping to 78,000 on day 4 of treatment. Testing later revealed the presence of heparin-dependent platelet antibodies, consistent with type 2 heparin-induced thrombocytopenia (HIT).
2) Treatment options for this patient include argatroban or lepirudin due to her hepatic dysfunction and renal insufficiency. Her anticoagulation will need to be closely monitored and continued for several months.
Acute liver failure can result from massive hepatocyte necrosis or severe impairment. It is defined by liver injury of less than 8 weeks, no chronic liver disease, and coagulopathy. Causes in children include viral infections, autoimmune disease, metabolic disorders, drugs, and unknown origins. Symptoms range from jaundice and coagulopathy to hepatic encephalopathy. Management involves supportive care, treating the underlying cause, and consideration of liver transplantation for severe cases. Prognosis depends on the cause and stage of encephalopathy, with survival rates varying from over 90% for acetaminophen overdose to less than 15% for subacute cases.
Hypercalcemia is commonly caused by primary hyperparathyroidism or malignancy. It can be life-threatening in severe cases. Diagnosis involves measuring serum calcium, PTH, and assessing for underlying causes. Treatment depends on the underlying condition but may involve surgery for hyperparathyroidism or addressing the malignancy. Complications can impact the kidneys, GI tract, cardiovascular system, muscles and bones.
Liver transplantation; notes of DM/DNB/SpecialistsPratap Tiwari
Liver transplantation; extensive notes of DM/DNB/Specialists. This was my notes for my exam compiled from several sources, credit goes to original authors. This is just for quick revision
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
Seminar on acute lymphoblastic leukemia by Dr. Prachi KalraMAMC,Delhi
This document provides information about acute lymphoblastic leukemia (ALL):
- ALL is a cancer of the white blood cells that starts from immature lymphocytes in the bone marrow. It causes a buildup of abnormal lymphocytes that crowds out normal blood cell production.
- Symptoms include fever, bleeding, bone pain, swollen lymph nodes and organs, and neurological issues. Diagnosis involves blood tests, bone marrow biopsy, immunophenotyping and cytogenetic analysis.
- Treatment involves supportive care, induction chemotherapy to achieve remission, consolidation therapy to further reduce cancer cells, and long-term maintenance therapy to prevent relapse. Prognosis depends on risk factors like age and specific genetic abnormalities.
This document discusses renal failure in patients with cirrhosis. It defines hepatorenal syndrome (HRS) as a type of renal failure seen in cirrhosis without intrinsic kidney abnormalities. HRS is classified into types 1-4 depending on severity and timeline of onset. Type 1 has the worst prognosis with median survival of 1-2 weeks. Treatment involves vasoconstrictors like terlipressin combined with albumin for volume expansion. For refractory ascites, large volume paracentesis with albumin is first line, while TIPS may be considered. Renal replacement therapy alone does not improve outcomes in HRS but may be used as a bridge to liver transplantation, which is the definitive treatment for HRS
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.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
This document discusses the approach and management of thrombocytopenia and immune thrombocytopenic purpura (ITP). It defines thrombocytopenia and its causes, provides diagnostic criteria for ITP, and outlines treatment approaches including corticosteroids, IVIG, anti-D, thrombopoietin receptor agonists, splenectomy, rituximab, and experimental therapies. It also addresses management of severe bleeding, pregnancy-associated thrombocytopenia, and thrombocytopenia in the settings of HIV and hepatitis C infection.
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 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.
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.
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.
Heart failure and liver dysfunction By Dr. Vaibhav Yawalkar MD,DM Cardiologyvaibhavyawalkar
1) Heart failure and liver disease often coexist due to shared risk factors and pathophysiological mechanisms that affect both organs.
2) Impaired cardiac function can lead to hepatic dysfunction through liver hypoperfusion and congestion, while liver disease can also cause cardiomyopathy.
3) Understanding the cardio-hepatic interactions and exploring therapeutic targets like liver X receptors and the gut microbiome may help manage patients with both heart failure and liver disease.
Tumour lysis syndrome (TLS) is a metabolic condition caused by the breakdown of malignant cells, characterized by electrolyte abnormalities like hyperuricaemia, hyperphosphataemia, hyperkalaemia and hypocalcaemia. It can occur before, during or after treatment for malignancy. Clinical TLS involves organ failure from electrolyte imbalances. Risk factors include extensive tumour burden and poor renal function. Prevention involves monitoring for symptoms and electrolyte levels before and after therapy. Treatment focuses on correcting electrolyte abnormalities through hydration, diuretics, binders, insulin therapy and dialysis if needed.
This document discusses thrombotic thrombocytopenic purpura (TTP). It begins by presenting a case of a 32-year-old woman presenting with headaches, difficulty speaking and moving her tongue, and numbness. Her exam and labs show thrombocytopenia and schistocytes. The document then discusses the differential diagnosis, epidemiology, terminology, definitions, types, presentations, investigations, and treatment of TTP, with a focus on plasma exchange therapy to remove antibodies and replace deficient ADAMTS13 protease.
Cardiorenal syndrome (CRS) refers to conditions where acute or chronic dysfunction of the heart or kidneys induces dysfunction of the other organ. CRS is classified into 5 subtypes depending on whether cardiac or renal dysfunction occurs first, and whether it is acute or chronic. Type 1 involves acute cardiac dysfunction leading to acute kidney injury. Type 2 involves chronic cardiac dysfunction resulting in worsening chronic kidney disease. Type 3 involves acute kidney injury leading to cardiac issues. Type 4 involves chronic kidney disease contributing to cardiac problems. Type 5 involves systemic conditions affecting both organs. Early diagnosis and treatment tailored to the CRS subtype is important for improving outcomes.
This document discusses thrombocytopenia, providing information on:
- Causes including decreased platelet production, sequestration, and increased destruction.
- Idiopathic thrombocytopenic purpura (ITP), the most common cause in children, which is an autoimmune condition where antibodies destroy platelets.
- Clinical presentation, diagnosis, treatment including corticosteroids, IVIG, and splenectomy for severe or chronic cases.
- Other considerations like drug-induced thrombocytopenia and conditions involving nonimmune platelet destruction.
This document discusses Heparin-Induced Thrombocytopenia (HIT). It covers the immunology of HIT including how antibodies form against platelet factor 4. It describes the clinical presentations of HIT focusing on the 4Ts criteria of thrombocytopenia, timing of platelet drop, thrombosis, and other causes. It discusses laboratory diagnosis using assays to detect antibodies. The document concludes with sections on treatment options including alternative anticoagulants and managing HIT in different clinical scenarios.
1) The patient's platelet count decreased while receiving heparin therapy, with counts dropping to 78,000 on day 4 of treatment. Testing later revealed the presence of heparin-dependent platelet antibodies, consistent with type 2 heparin-induced thrombocytopenia (HIT).
2) Treatment options for this patient include argatroban or lepirudin due to her hepatic dysfunction and renal insufficiency. Her anticoagulation will need to be closely monitored and continued for several months.
Acute liver failure can result from massive hepatocyte necrosis or severe impairment. It is defined by liver injury of less than 8 weeks, no chronic liver disease, and coagulopathy. Causes in children include viral infections, autoimmune disease, metabolic disorders, drugs, and unknown origins. Symptoms range from jaundice and coagulopathy to hepatic encephalopathy. Management involves supportive care, treating the underlying cause, and consideration of liver transplantation for severe cases. Prognosis depends on the cause and stage of encephalopathy, with survival rates varying from over 90% for acetaminophen overdose to less than 15% for subacute cases.
Hypercalcemia is commonly caused by primary hyperparathyroidism or malignancy. It can be life-threatening in severe cases. Diagnosis involves measuring serum calcium, PTH, and assessing for underlying causes. Treatment depends on the underlying condition but may involve surgery for hyperparathyroidism or addressing the malignancy. Complications can impact the kidneys, GI tract, cardiovascular system, muscles and bones.
Liver transplantation; notes of DM/DNB/SpecialistsPratap Tiwari
Liver transplantation; extensive notes of DM/DNB/Specialists. This was my notes for my exam compiled from several sources, credit goes to original authors. This is just for quick revision
hepatorenal syndrome is a one of the complication of cirrhosis of liver. It causes hepatic decompensation of liver. It has high risk of mortality. HRS has two types and type 1 usually present as a acute kidney injury. so, at first HRS should exclude from AKI. HRS type 2 present as a refractory ascites. As this has worst prognosis, only valuable management is liver transplantation.
Seminar on acute lymphoblastic leukemia by Dr. Prachi KalraMAMC,Delhi
This document provides information about acute lymphoblastic leukemia (ALL):
- ALL is a cancer of the white blood cells that starts from immature lymphocytes in the bone marrow. It causes a buildup of abnormal lymphocytes that crowds out normal blood cell production.
- Symptoms include fever, bleeding, bone pain, swollen lymph nodes and organs, and neurological issues. Diagnosis involves blood tests, bone marrow biopsy, immunophenotyping and cytogenetic analysis.
- Treatment involves supportive care, induction chemotherapy to achieve remission, consolidation therapy to further reduce cancer cells, and long-term maintenance therapy to prevent relapse. Prognosis depends on risk factors like age and specific genetic abnormalities.
This document discusses renal failure in patients with cirrhosis. It defines hepatorenal syndrome (HRS) as a type of renal failure seen in cirrhosis without intrinsic kidney abnormalities. HRS is classified into types 1-4 depending on severity and timeline of onset. Type 1 has the worst prognosis with median survival of 1-2 weeks. Treatment involves vasoconstrictors like terlipressin combined with albumin for volume expansion. For refractory ascites, large volume paracentesis with albumin is first line, while TIPS may be considered. Renal replacement therapy alone does not improve outcomes in HRS but may be used as a bridge to liver transplantation, which is the definitive treatment for HRS
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.
A simple description of a less understood topic in Intensive Care Medicine. Aim to make understanding and management easy for the residents and prevention steps for all ICU workers.
This document discusses the approach and management of thrombocytopenia and immune thrombocytopenic purpura (ITP). It defines thrombocytopenia and its causes, provides diagnostic criteria for ITP, and outlines treatment approaches including corticosteroids, IVIG, anti-D, thrombopoietin receptor agonists, splenectomy, rituximab, and experimental therapies. It also addresses management of severe bleeding, pregnancy-associated thrombocytopenia, and thrombocytopenia in the settings of HIV and hepatitis C infection.
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.
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.
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 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.
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 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.
This document discusses hematological emergencies and tumor lysis syndrome. It provides classifications of hematological emergencies and describes tumor lysis syndrome, including its causes, risk factors, clinical manifestations, and treatments like hypouricemic drugs, hydration, and renal replacement therapy. It also covers superior vena cava syndrome, its causes, clinical features, grading of severity, diagnosis using imaging, and treatments including supportive care, stenting, and glucocorticoids.
1. Chronic cholestasis can be caused by intrahepatic or extrahepatic conditions. Common intrahepatic causes include primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and drug-induced liver injury (DILI).
2. PBC is an autoimmune disease characterized by progressive destruction of intrahepatic bile ducts, presence of antimitochondrial antibodies (AMA), and histologic findings of florid duct lesions on liver biopsy. PBC diagnosis requires two of three criteria: cholestatic liver enzymes, AMA positivity, or liver biopsy consistent with PBC.
3. PSC is a chronic inflammatory condition of
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.
This document discusses common childhood cancers, focusing on leukemias. It provides details on the types and subtypes of leukemia, risk factors, clinical presentation, evaluation, and management. The main types discussed are acute lymphoblastic leukemia (ALL), which is the most common childhood cancer, and acute myeloid leukemia (AML). The management of ALL involves induction therapy to achieve remission, CNS prophylaxis to prevent spread to the brain, intensification therapy, and maintenance therapy to prevent relapse.
This document provides an overview of acute liver failure (ALF), including its definition, classification, etiology, clinical manifestations, diagnosis, treatment, complications, prognosis, and liver support devices. ALF is defined as evidence of coagulation abnormalities and mental alterations in a patient without preexisting cirrhosis within 26 weeks of illness onset. Common etiologies in India include hepatitis E, drug-induced liver injury, and acetaminophen toxicity. Presentation may include jaundice, coagulopathy, and hepatic encephalopathy. Treatment involves supportive care and managing complications such as cerebral edema. Prognosis is assessed using scoring systems like King's College criteria, with liver transplantation indicated for those who do not recover spontaneously.
Oncologic Emergencies and Symptom Managementflasco_org
1) Oncologic emergencies include conditions like hypercalcemia, tumor lysis syndrome, SIADH, hyperviscosity states, and increased intracranial pressure that require immediate medical intervention.
2) Tumor lysis syndrome occurs when cancer cells die off rapidly, releasing electrolytes and metabolites that can overwhelm the kidneys, potentially causing renal failure, arrhythmias or seizures. It is treated by managing individual electrolyte abnormalities and renal failure.
3) Increased intracranial pressure in cancer patients can be caused by vasogenic edema, hemorrhage, or obstruction of cerebrospinal fluid flow. Symptoms include headache, vomiting and altered mental status. Treatment involves steroids
This document provides information on acute pancreatitis, including:
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Leukemia are neoplastic disorders of the hematopoietic system characterized by aberrant or arrested differentiation. There are two main types - acute and chronic leukemias. Acute leukemias are further classified as myeloid or lymphoid based on the lineage of the malignant cells. Chromosomal abnormalities are detected in the majority of acute leukemia cases and correlate with specific disease subtypes and clinical outcomes. Treatment involves induction chemotherapy followed by consolidation therapy and stem cell transplantation for eligible patients, with cure rates varying based on disease risk factors.
This document provides an overview of various oncologic emergencies including hypercalcemia, tumor lysis syndrome, SIADH, hyperviscosity states, increased intracranial pressure, spinal cord compression, superior vena cava syndrome, neutropenic fever, and other urgencies. For each condition, it discusses causes, clinical manifestations, diagnosis, and treatment approaches. The goal is to educate medical professionals about emergency presentations that may occur in cancer patients and how to appropriately manage these critical situations.
complete information about the cancer condition that is leukemia - introduction, definition, etiology and causes, pathophysiology ,types, clinical manifestations, diagnosis, nursing management, medical management, nursing research .
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
3. INTRODUCTION
• Tumor lysis syndrome is an oncometabolic
emergency resulting from rapid cell death.
• Tumor lysis syndrome can occur as a
consequence of tumor targeted therapy or
spontaneously.
• TLS comprises a clinicolaboratory
derangement of cellular metabolism, which
can lead to AKI, cardiac arrhythmias, seizures,
and death
4. INTRODUCTION
• Cellular death mediated by treatment
targeted at cancer (chemotherapy or another
pharmacological antitumor intervention,
embolization of tumor or radiation therapy) or
spontaneous cellular death in rapidly dividing
cancer cells (which is known as spontaneous
TLS) leads to an efflux of cellular material rich
in potassium, phosphorus, and uric acid into
the bloodstream.
5. DEFINITION
• Hande and Garrow
– first initiated a definition of the clinical and pathologic
characteristics of patients at risk for developing TLS.
– retrospective analysis of 102 patients with non-Hodgkin
lymphoma (NHL),
– laboratory TLS (LTLS) or clinical TLS (CTLS).
• Cairo and Bishop modification
– This system defines LTLS when two or more of the
following abnormalities are met within 3 days before or 7
days after the initiation of chemotherapy:
25%decrease from baseline in serum calcium, and/or
25% increase from baseline in the serum values of uric acid,
potassium, or phosphorous.
6. DEFINITION
• CTLS when LTLS is accompanied by one or
more clinical manifestations such as cardiac
arrhythmia, death, seizure, or AKI with an
elevated serumcreatinine.1.5 times upper
limit of normal.
• There is a third class which specifies patients
with normal laboratory and clinical
parameters as having no LTLS or CTLS.
9. Limitation of Cairo-Bishop grading
• Although this grading system attempts to provide
uniform definitions to TLS severity, it is not widely
used in clinical practice.
• Patients with TLS may not always have two or
more abnormalities present at once, but one
metabolic derangement may precede another
• a 25% change from baseline may not always be
significant if it does not result in a value outside
the normal range
• cannot be applied to spontaneous TLS, which is
common with high-risk malignancies, as
chemotherapy is a required criterion for LTLS and
CTLS.
10. Limitation of Cairo-Bishop grading
• From a renal standpoint, Wilson and Berns
have noted that defining AKI on the basis of a
creatinine value .1.5 times the upper limit of
normal does not clearly distinguish CKD from
AKI.
• Thus, they propose using established
definitions of AKI in CTLS such as an absolute
0.3 mg/dL increase or relative 50%increase in
creatinine over baseline
11. EPIDEMIOLOGY AND RISK FACTORS
• most common in NHL, particularly Burkitt-type lymphoma (BTL), as
well as other hematologic malignancies, such as ALL and AML and
less common in CLL,CML and MM
• Rare in solid tumors. Criteria for presence:
large tumor burden,
metastatic disease, specifically in the liver,
short doubling time,
increased chemosensitivity,
elevated uric acid and
Elevated lactate dehydrogenase (LDH)
• small-cell carcinoma of the lung, germ cell tumors, neuroblastoma,
and breast carcinoma
• Usually associated with cytotoxic chemotherapy,irradiation and
chemoembolism
• It can also occur spontenously
12. EPIDEMIOLOGY AND RISK FACTORS
• using the Hande-Garrow classification, LTLS was seen in
42% of patients, with CTLS occurring only in 6%
• Mato et al. studied 194 patients receiving induction
therapy for AML and found a TLS incidence of 9.8%.
• In amixed adult and pediatric study of 788 European
patients with acute leukemia or NHL, the overall
incidence of LTLS and CTLS was 18.9% and 5%,
respectively
• Wössman et al. reviewed the incidence and
complications of 1,791 children with NHL and reported
an overall incidence of 4.4%, of which 26% had B-cell
ALL (B-ALL).
13. EPIDEMIOLOGY AND RISK FACTORS
• Risk Stratification
– Elderly
– Nephrotoxic Drugs e.g NSAIDS,ACEi and ARBs
– a baseline increase in serum uric acid,
phosphorus, potassium, and LDH
– general comorbid conditions such as cardiac
disease, diabetes mellitus, and renal disease
14. clinical risk stratification proposed by
Cairo et al
• The high risk group of cancers
– advanced Burkitt’s lymphoma/leukemia or
– early stage disease with elevated baseline LDH,
– acute lymphocytic leukemia (ALL) with white blood
cell (WBC) count ≥ 100000 or less if the baseline
elevation of LDH is twice the upper limit of normal
(ULN),
– acute myeloid leukemia (AML) with WBC count ≥
100000,
– diffuse large B-cell lymphoma with an elevated
baseline LDH of twice ULN, and bulky disease.
15. clinical risk stratification proposed by
Cairo et al
• Intermediate risk malignancies include
– AML with a WBC between 25000 and 100000,
– ALL with WBC < 100000 and an LDH of less than
twice ULN,
– early stage Burkitt lymphoma/leukemia with an
LDH of less than twice ULN, and
– diffuse large B-cell lymphoma with a baseline
increase in LDH of twice ULN but non-bulky
disease.
16. clinical risk stratification proposed by
Cairo et al
• Low risk diseases include
– indolent lymphomas,
– chronic lymphocytic leukemia,
– chronic myeloid leukemia in the chronic phase,
– AML with WBC count < 25000 and an LDH
elevated to less than twice ULN,
– multiple myeloma, and
– solid cancers.
17. PATHOPHYSIOLOGY
Hyperuricemia
• The nucleic acids adenine and guanine are metabolized
to xanthine, which is further metabolized by xanthine
oxidase to the water-insoluble uric acid.
• Because humans lack a functional gene for urate
oxidase (uricase), which further metabolizes uric acid
to the freely soluble and excretable allantoin, patients
with high-risk malignancy are susceptible to rapid
increases in serum uric acid.
• When the capacity to transport luminal uric acid is
overwhelmed, there is potential for uric acid to
crystallize within the tubular lumen.
18. • Uric acid crystals can cause direct tubular injury by
– obstruction,
– induction of chemokine-mediated inflammation from
monocyte chemoattractant protein-1 (MCP-1) and
macrophage migration inhibition factor (MIF) .
– crystal-independent mechanisms which target
hemodynamics.
increased peritubular capillary pressures,
Increased vasoconstriction, and
decreased blood flow
– Uric acid may also prevent recovery from AKI in TLS,since it
inhibit proximal tubule cell proliferation.
19.
20. Hyperkalemia
• Massive tumor cell lysis releases potassium into
the extracellular environment,
• leading to severe hyperkalemia when uptake
capacity by muscle and liver is exceeded,
especially in the setting of CKD or AKI.
• Muscle weakness may be the initial symptom, but
cardiac arrhythmia, manifested initially by peaked
Twaves,widened QRS complexes, and sine waves,
is the feared complication.
21. Hyperphosphatemia and hypocalcemia
• cell lysis releases significant amounts of bisphosphate
• malignant hematologic cells may contain four times more intracellular
phosphate in comparison to normal mature lymphoid cells
• Because phosphorus excretion is tied to kidney function,
hyperphosphatemia occurs when the kidney’s excretory capacity is
overwhelmed.
• Thus, preexisting CKD or AKI enhances risk for hyperphosphatemia with
TLS.
• Spontaneous tumor lysis, however, is less commonly associated with
hyperphosphatemia and may be due to rapid uptake of extracellular
phosphate by residual highly metabolically active tumor cells.
• Hyperphosphatemia may cause nausea, vomiting, diarrhea, or lethargy,
but
• it exerts its predominant toxicity by binding to calcium cations.
• This results in secondary hypocalcemia and its down stream
neuromuscular and cardiovascular effects such as cramps, hypotension,
tetany, and arrhythmias.
• Additionally, calcium–phosphate precipitates may deposit in tissues, as
seen in nephrocalcinosis, including the renal interstitium.
22. AKI
• AKI in TLS may be either due to the aforementioned
effects of acute urate nephropathy or
hyperphosphatemic nephrocalcinosis affecting the
renal tubulointerstitium or acombination of the two.
• Some studies have suggested that a urine uric acid to
creatinine ratio of >1may be specific to uric acid
nephropathy
• AKI due to TLS may be asymptomatic or include
symptoms of uremia, including nausea, vomiting, and
lethargy.
23. MANAGEMENT
Prophylaxis and monitoring
• recognition of risk factors and close laboratory and clinical
monitoring.
• Patients at highest risk of developing TLS require intensified
monitoring with more frequent electrolyte checks.
• Patients with high-risk Disease may be prone to lactic acidosis from
massive tumor cell necrosis.
• Because acidosis inhibits uric acid excretion prompt recognition and
correct of acidosis may prevent or ameliorate uric acid
nephropathy.
• Nonsteroidal anti-inflammatory drugs, iodinated radiocontrast dye,
and other potentially nephrotoxic therapeutic agents should be
avoided to abrogate the risk of AKI from TLS.
24. Volume expansion
• Delivery of crystalloid intravenous fluids (IVFs)
is recommended
• Volume expansion supports adequate
intravascular volume and Renal blood flow,
which maintain glomerular filtration.
• High-dose IVFs up to 3 L have been
recommended, for a target urine output of
atleast 2 mL/kg/h.
25. Urinary alkalinization
• increasing urine pH from 5 to 7 can increase
the solubility of uric acid >10-fold
However, urinary alkalinization decreases calcium–
phosphate solubility , thereby exacerbating its
precipitation and deposition.
Furthermore, if urinary alkalinization results in rising
serum pH, free calcium may bind albumin more avidly
and further exacerbate hypocalcemia .
Thus, urinary alkalinization is not recommended in the
management of TLS .
26. Allopurinol
• Allopurinol is converted in vivo to oxypurinol and as a xanthine analog acts as a
competitive inhibitor of xanthine oxidase and blocks the conversion of purines to
uric acid.
• This prevents hyperuricemia but does not treat preexisting hyperuricemia
Furthermore, because oxypurinol also inhibits the conversion of xanthine to uric acid, serum
and urine xanthine levels may rise and precipitate xanthine crystal deposition in the renal
tubules and xanthine-induced obstructive nephropathy
• Administration of allopurinol is recommended for prophylaxis in patients with low
and intermediate risk of developing TLS .
• Because oxypurinol excretion is by the kidney, dose adjustments are necessary for
patients with CKD and AKI.
• Allopurinol has been associated with a hypersensitivity syndrome with rash, acute
hepatitis, and eosinophilia .
• Allopurinol reduces the clearance of purine-based chemotherapeutic agents such
as 6-mercaptopurine and azathioprine
• It may also interact with azathioprine and cyclophosphamide in potentiating
severe bone marrow suppression
27. Febuxostat
• Febuxostat is a novel xanthine oxidase inhibitor lacking the
hypersensitivity profile of allopurinol.
• Because it is metabolized to in active metabolites by the
liver, adjustment for reduced GFR is not necessary.
• It has been proposed as a viable alternative to allopurinol in
TLS prophylaxis for patients with allopurinol
hypersensitivity or renal dysfunction.
• A recently completed phase III study of febuxostat versus
allopurinol in TLS prevention found significantly lower
serum uric acid in the febuxostat but found no significant
difference in serum creatinine change compared with
allopurinol .
28. Rasburicase
• Rasburicase (Elitek) is an Aspergillus-derived recombinant urate
• Rasburicase catalyzes the conversion of uric acid to allantoin, carbon dioxide, and
hydrogen peroxide .
• Allantoin is 5- to 10-fold more soluble than uric acid and is readily excreted.
• rasburicase should be used for prophylaxis in patients with high risk of developing
TLS .
• Rasburicase does not require dosing adjustment for GFR and is not known to have
any known clinically relevant drug– drug interactions .
• Adverse reactions are rare but may include rash, increased liver enzyme levels,
headaches, fever,
• vomiting, and nausea .
• Rasburicase is active ex vivo, so blood samples for serum uric acid levels must be
stored on ice to avoid erroneously low results .
• Patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency can develop
significant methemoglobinemia and hemolysis due to oxidative stress triggered by
hydrogen peroxide .
• Thus, patients should have G6PD status tested prior to starting rasburicase.
29. RRT
• The need for renal replacement has significantly reduced since the
advent of rasburicase, but about 1.5%of children and 5% of adults
require dialysis during induction therapies.
• Indications for RRT are similar to those for AKI from other causes,
but due to the rapid onset of the clinical manifestations of TLS, the
threshold for initiating dialytic therapies is lower than in other
situations.
• Although intermittent hemodialysis (IHD) may be sufficient for most
patients, continuous RRT (CRRT) at high dialysate or replacement
fluid flow rates (.3-4 L/h) may be necessary in those patients with
severe TLS who experience rebound in serum potassium and
phosphorous levels with IHD
30. PROGNOSIS
• There are many confounding factors that impact clinical
outcomes in patients with malignancies, particularly in
those who have TLS, but AKI appears to be a significant
predictor of short- and long-term mortality from TLS.
• A study comparing hematologic cancer patients without AKI
to patients with AKI showed significantly lower hospital
mortality (7% and 21%, respectively) and 6-month
mortality (51% and 66%, respectively) in patients without
AKI.
• TLS is most common during initial presentation of disease
because relapsed malignancies are significantly more
chemoresistant.
31. CONCLUSIONS
• TLS is a common oncologic emergency that
requires immediate diagnosis and prompt
treatment to avoid morbidity and mortality.
• Understanding the diagnostic criteria for TLS,
knowing the tumor types at high risk for TLS,
and instituting prophylactic and treatment
measures are essential for the nephrologist
who treats patients with malignant diseases.
32. REFERENCES
• CairoMS, Bishop M. Tumor lysis syndrome: New therapeutic strategies and
classification. Br J Haematol 127: 3–11, 2004
• Cairo MS, Coiffier B, Reiter A, Younes A, Baruchel A, Bosly A, Goldman SC,
Leverger G, Ohyashiki K, Panagiotidis P, Pession A, Pui CH, Ribera JM, Rosti
G, Rule S, Tsukimoto I, Zinzani PL. Recommendations for the evaluation of
risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children
with malignant diseases: An expert TLS panel consensus. Br J Haematol
149: 578–586, 2010
• Hsieh PM, Hung KC, Chen YS. Tumor lysis syndrome after transarterial
chemoembolization of hepatocellular carcinoma: Case reports and
literature review. World J Gastroenterol 15: 4726–4728, 2009
• Cohen LF, Balow JE, Magrath IT, Poplack DG, Zeigler JL. Acute tumor lysis
syndrome: A review
• Harrisons principle of internal medicine 20th edition
• Slide share
Editor's Notes
However, serum calcium levels typically decrease in patients with TLS because of its binding to excess phosphorus.
this definition of
CTLS assumes that the clinical manifestations are not caused directly by the therapeutic agent.
Small cell CA doubling time= 86days
Germ call tumors doubling time= 0.5-80 days
Neuroblastoma doubling time= 4.2days
Nephroblastoma doubling time= 7.8 days
Breast CA doubling time= 44-1800DAYS
Most incidence data are from older, retrospective studies that precede the Cairo-
Bishop classification, so there is considerable heterogeneity in the data.
An older age is associated with a reduction in the glomerular filtration and a decrease in the renal reserve, and may complicate volume replacement therapy due to higher rates of cardiac dysfunction.
LDH = 140-280 U/L
Uric acid is freely filtered at the glomerulus, and handling in the renal proximal tubule is a combination of reabsorption and secretion via the luminal urate/anion exchanger urate transporter 1 (URAT-1) and the basolateral organic anion transporter (OAT) .
URAT-1 is an apical membrane transporter and exchanges anions for urate absorption from the tubular lumen. It is critical in regulating urate levels and is targeted by uricosuric and antiuricosuric agents.
Clinically, hyperuricemia is unlikely to cause symptoms because urinary crystallization of uric acid does not result in the renal colic, which is typical of uric acid nephrolithiasis.
K=5.5-6.5 (tall, peaked T waves with a narrow base, best seen in precordial leads [3] ; shortened QT interval; and ST-segment depression.)
K= 6.5 – 8(Prolonged PR interval,Decreased or disappearing P wave,Widening of the QRS ,Amplified R wave)
but another study has noted high uric acid to creatinine ratios in AKI from other etiologies
Diuretics may be necessary if patients develop volume overload, but routine use is not recommended to avoid volume depletion.
The FDA-approved dosing guidelines recommend 0.2 mg/kg in 50 mL normal saline as a 30-minute intravenous infusion once daily for up to 5 days.