Description
This oncology presentation on Tumour Lysis Syndrome (TLS) provides a detailed overview of its definition, epidemiology, risk factors, pathophysiology, clinical presentation, and management. The material defines TLS as a metabolic emergency resulting from rapid tumor cell lysis, commonly associated with hematologic malignancies like acute lymphoblastic leukemia and Burkitt lymphoma, leading to hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury. Key risk factors include high tumor burden, rapidly dividing tumors, preexisting renal impairment, and dehydration. Clinical features encompass neuromuscular symptoms, cardiac arrhythmias, oliguria, and renal dysfunction. Management focuses on risk assessment, prophylaxis with hydration and allopurinol or rasburicase, and targeted therapy for metabolic derangements. This resource is essential for medical students, oncology trainees, and practitioners in Zambia, offering structured, exam-focused content for understanding and managing TLS within a tertiary medical education setting. Download these comprehensive notes for thorough preparation on oncologic emergencies.
What's inside
TUMOUR LYSIS SYNDROME Presenter: Tiza Chipungu Moderator: Dr Mwanza Contents Definition Epidemiology Risk Factors Pathophysiology Clinical presentation Investigations Treatment Approached Definition TLS is a condition that occurs when a large number of cancer cells die within a short period, releasing their contents such as ions and metabolic by products in to the blood. Can either be spontaneous or in response to therapy. It is typically associated with the response to treatment in the following tumors; ALL, non-Hogkin lymphomas like Burkitt Lymphoma. Classification Epidemiology The incidence of clinical tumor lysis syndrome is estimated at 3-7% in leukemia and 4-11% in lymphomas overall Risk Factors Patients with a large “tumor burden” of cancer cells Hematologic malignancies Tumors that typically have rapidly dividing cells, such as acute leukemia or high-grade lymphoma Tumors that are highly responsive to therapy Patients within a week of starting cancer treatment Preexisting neuropathy Dehydration Pre-existing hyperuricaemia or hyperphosphatemia Pathophysiology Pathophysiology There is rapid lysis of tumour cells which results in the release of massive quantities of intracellular contents such as potassium, phosphate, and nucleic acids that can be metabolized to uric acid, into the systemic circulation. The metabolic consequences include hyperkalemia, hyperphosphatemia, secondary hypocalcemia, hyperuricemia, and acute kidney injury. Clinical Presentation Hyperkalemia: Potassium> 6.0mmol/litre Weakness Paresthesia Arrhythmias Myalgias Clinical Presentation Secondary Hypocalcemia; Corrected calcium<1.75mmol/litre or ionized calcium<0.3mmol/litre Arrhythmias Seizures Neuromuscular irritability (tetany, paresthesias, muscle twitching,Trousseau’s sign, Chvostek’s sign, laryngospasm, or bronchospasm), hypotension, or heart failure . Clinical Presentation Acute Kidney Injury: Increase in the serum creatinine level of 0.3 mg/dl (26.5 μmol/liter) oliguria, defined as an average urine output of <0.5 ml/kg/hr for 6 hr Uric acid nephropathy Dysuria Flank pain Hematuria Investigations NOTE: Early recognition of signs and symptoms Bloods; serum sodium, potassium, chloride and bicarbonate. Urine pH and output Chest x-ray Ultrasound or CT scan of abdomen and retroperitoneum Cardiac monitoring Treatment Approach Risk assessment Prophylaxis Therapy Prophylaxis Hydration Allourinol or Rasburicase 24 hrs before therapy Therapy Aluminium hydroxide for hyperphosphotamia Rasburicase for hyperuricemia Allopurinol Intravenous fluid Treatment
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