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Oncologies_Emergency.pptx
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- 2. • Tumour lysissyndrome • Hyponatremia • Hypokalemia • Hypercalcemia Metabolic emergencies • hyperleucocytosis • coagulopathy • thrombocytopenia • Severe anemia Haematological emergencies Superior vena cava obstruction • Febrile neutropenia • typhilitis Infection • Spinal cord compression • Increase intracranial pressure and brain herniation • cva Neurological complication • Pancreatitis • ATRA SYNDROME Others
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- 4. DEFINITION • Massive tumourcell death with rapid release of intracellular metabolites, which exceeds the excretory capacity of the kidneys leading to acute renal failure. Can occur before chemotherapy is started. • Risk factor include large tumor burden/bulky volume, cancers that rapidly divide or cancers that are extremely sensitive to chemotherapy .Common in Iymphoproliferative tumours with abdominal involvement (e.g. B cell/ T cell Iymphoma, leukaemias and Burkitt’s Iymphoma)
- 6. CHARACTERISTICS: • Hyperuricaemia • Releaseof intracellular purines increase uric acid • Hyperkalaemia • Occurs secondary to tumour cell Iysis itself or secondary to renal failure from uric acid nephropathy or hyperphosphataemia. • Hyperphosphataemia with associated hypocalcaemia • Most commonly occurs in Iymphoproliferative disorders because Iymphoblast phosphate content is 4 times higher than normal lymphocytes. • Causes: Tissue damage from CaPO₄ precipitation. Occurs when Ca X PO₄ > 60 mg/dl. Results in renal failure, pruritis with gangrene, eye and joint inflammation Hypocalcaemia leading to altered sensorium, photophobia, neuromuscular irritability, seizures, carpopedal spasm and gastrointestinal symptoms
- 7. Howard et al.,NEJM, 2011
- 8. complication * Close attentionto symptoms of electrolyte abnormalities: Abdominal pain Back pain Vomiting Cramps Diarrhea Dehydration Muscle spasms Tetany, seizures
- 9. Management (Prevention): To beinstituted in every case of acute leukaemia or Iymphoma prior to induction chemotherapy. • Hydration : Double hydration - 125ml/m²/hr or 3000ml/m²/day. - No added potassium. • Alkalization of urine: Adding NaHCO₃ at 150 - 200 mmol/m²/day (3 mls/kg/day NaHCO₃ 8.4%) into IV fluids to keep urine pH 7.0 - 7.5. - Avoid over alkalinization as this may aggravate hypocalcemia and cause hypoxanthine and xanthine precipitation. It can also cause precipitation of calcium phosphate if pH > 8. Monitor urine pH and VBG 8 hourly. If urine pH < 7.0 , consider increasing NaHCO₃ infusion. This can only be done if HCO₃ in the blood is below normal range. Otherwise, have to accept that some patients just cannot alkalinise their urine. • Allopurinol : 10mg/kg/day, max 300mg/day. • May have to delay chemotherapy until metabolic status stabilizes. • Close electrolyte monitoring: BUSE, Ca²⁺, PO₄, uric acid, creatinine, bicarbonate. • Strict I/O charting. Ensure adequate urine flow once hydrated. Use diuretics with caution. Maintain urine output at least 3 mL/kg/hr – Lasix 0.5-1 mg/kg – Mannitol 0.5 g/kg
- 10. Management (Treatment) • hyperkalaemia– oral kalimate,lytic cocktail, dialysis in severe cases. • Diuretics. • Hypocalcaemia management depends on the phosphate level: If phosphate is raised, then management is directed to correct the high phosphate. If phosphate is normal or if child is symptomatic, then give replacement IV calcium. If hypocalcaemia is refractory to treatment, exclude associated hypomagnesaemia. • Dialysis if indicated. Haemodialysis most efficient at correcting electrolyte abnormalities. Peritoneal dialysis is not effective in removing phosphates.
- 11. Pediatric Emergency MedicineReports / May 2011/www.ahcmedia.com
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- 14. • Occurs inacute leukaemia. Defined as TWBC > 100 000 / mm³. • Leukostasis - Blasts lack deformability • Increased viscosity > WBC aggregates > thrombi especially in small veins causing obstruction • Excessive leukocytes competes for oxygen; damages vessel wall causing bleeding. • Can be fatal (greatest risk at WBC > 300K) CNS hemorrhage, thrombosis • Pulmonary Leukostasis - Affects the lungs due to pulmonary infiltrates. May cause dyspnoea, hypoxaemia and right ventricular failure. • Affects the central nervous system causing headaches, papilloedema, seizures, haemorrhage or infarct. Associated : - In acute lymphoblastic leukaemia (ALL) with high risk of tumour Iysis. - In AML with leucostasis (esp monocytic). - Seen in 10% ALL and 15-20% AML
- 15. There are nodiagnostic tests or criteria for leukostasis. Clinicians must have a high index of suspicion in patients who are at risk as defined above. Respiratory and CNS status must be reviewed regularly. Discuss with PTC consultants early if leukostasis is suspected.
- 16. MANAGEMENT A-B-C • Hydration Tofacilitate excretion of toxic metabolites. To reduce blood viscosity. Avoid increasing blood viscosity. • Strict i/o chart • Daily weight bd/od • Ix: FBC, ca, po4 ,mg ,uric acid, urea creatinine, LDH • Cautious in use of packed cell transfusion(increase viscosity) and diuretics – not recommend unless in life threatening condition. • During induction in hyperleukocytosis, keep platelet >20 000/mm³ and coagulation profile near normal Consider platelet transfusion if <20000/mm3 – prevent haemorrhage • If WBC rises rapidly / does not drop quickly, consider cytoreduction Steroids : • Hydoxyurea • Leukopheresis • Exchange transfusion *Exchange transfusions and leukopheresis should not be used alone as rapid rebound usually occurs. Concurrent drug treatment should therefore be initiated soonest possible.
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- 18. >> Pathologic processwhere there is generalized activation and dysregulation of the hemostatic system resulting in generation of microthrombi and consumption of platelets and clotting factors , this consumption result in Thrombosis, organ failure, Severe Bleeding • Patients at risk: APML and infection or sepsis • Causes: 1. Gram negative sepsis 2. Leukemia (AML M3,M5; ALL with high WBC) 3. Metastatic solid tumors • Signs & Symptoms: Bleeding, petechiae, purpura and laboratory derangements *AML especially M3 is associated with an initial bleeding diathesis from consumptive coagulopathy due to release of a tissue factor with procoagulant activity from cells. However the use of all-trans retinoic acid (Atra) has circumvented this complication.
- 19. Supportive Care Protocolversion 5.0 (August 2011), NHS foundation Management by protocol : • Platelet transfusions: 6 units / m² should increase platelets by 50,000 / mm³. • Fresh frozen plasma (FFP) or cryoprecipitate. • Vitamin K. • +/- Heparin therapy (10u/kg/hr) - controversial
- 20. Superior Vena Cava(SVC) Obstruction
- 21. • Superior VenaCava Syndrome (SVCS): Refers to signs and symptoms from compression, obstruction or thrombosis of the superior vena cava • Common in Non Hodgkin Lymphoma / Hodgkin Lymphoma / ALL . • Rarely: malignant teratoma, thymoma, neuroblastoma, rhabdomyosarcoma or Ewing’s may present with anterior or middle mediastinal mass and obstruction. • 50% associated with thrombosis. symptoms: facial swelling, upper body edema, cyanosis of the face or upper body, plethora, conjuctival suffusion, headache , shortness of breath,cough syncope. Signs: tacycardia, elevated venous pressure, vocal cord paralysis,dyspnea, horner syndrome #Sometimes no signs or symptoms until stressed
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- 23. Investigation: Diagnosis – History,Physical, CBC, CXR, CT, Echo 1. Recognition of symptoms and signs of SVC obstruction and avoidance of sedation and general anaesthesia. • Orthopnea, upper body edema, and dyspnea at rest have been associated with increased anesthesia risk. 2. Tissue diagnosis is important but should be established by the least invasive measure available. Risk of circulatory collapse or respiratory failure may occur with general anesthesia or sedation. 3. BMA. 4. Biopsy of superficial lymph node under local anaesthesia. 5. Measurement of serum markers e.g. alpha-fetoprotein. • Management • IV access (lower limbs if possible-a risk of exacerbation of facial swelling and cerebral oedema in SVC obstruction in upperlimb cannulae,bleeding due to increased intravascular pressure, aggravate SVC obstruction), keep hydration • Keep pt calm, minimal handling, no sedation • Upright, left lateral position with face mask O2 • Monitor and treat TLS • ECMO on standby if available • If tissue diagnosis is not obtainable, empiric treatment may be necessary based on the most likely diagnosis. Both chemotherapy and DXT may render histology uninterpretable within 48 hours, therefore biopsy as soon as possible • Primary mode of treatment is with steroids and chemotherapy if pathology due to Non-Hodkin Lymphoma • +/- DXT(adjuvant radiotherapy). • Intubate only for life threatening obstruction
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- 25. Febrile episodes inoncology patients must be treated with urgency especially if associated with neutropenia. Nearly all episodes of bacteraemia or disseminated fungal infections occur when the absolute neutorphil count (ANC) <500 /mm³. Risk increases maximally if ANC < 100 /mm³ and greatly reduced if the ANC > 1000 /mm³. Characterized by: • Fever (definition variable) • T>38.3° C x1 or • T>38.0°C x2 in a 24 hour period • Absolute neutrophil count (ANC) • < 500 or • < 1000 with expected decline • WBC count x (% segs + bands)
- 26. • Why arecancer pts at risk for life-threatening infection? • Chemotherapy Decreased number and function of immune cells • Radiation -further tissue injury and impairment of the body’s innate immunology • Surgeries • Breakdown of mucocutaneous barriers (indwelling catheter, etc) • Foreign bodies (CVL, grafts, etc.)
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- 29. other considerations: • Ifcentral line is present, culture from central line (both lumens); add anti-Staph cover e.g.Cloxacillin. • Repeated physical examination to look for new clues, signs and symptoms of possible sources. • Close monitoring of patient’s well-being – vital signs, perfusion, BP, I/O. • Repeat cultures if indicated • Investigative parameters, FBC, CRP, BUSE as per necessary. • In presence of oral thrush or other evidence of candidal infection, start antifungals. •Try to omit aminoglycoside and vancomycin if on cisplatinum - nephrotoxic and ototoxic. If required, monitor renal function closely.
- 30. references • PAEDIATRIC PROTOCOLSFor Malaysian Hospitals, 3rd edition • Paediatric Haematology & Oncology: Supportive Care Protocols NHS Foundation trust, 4th Edition version 1.0 • The Practical Journal of paediatric medical emergency, Volume 16, Number 5 / May 2011, www.ahcmedia.com
Editor's Notes
- #19 Acute Promyelocytic Leukaemia (APML) is a subtype of Acute Myeloid Leukaemia (AML). APML is most commonly associated with a swapping over (translocation) of chromosomes 15 and 17.
- #24 However, administrationof steroids may result in tumor lysis syndrome and may impair the ability to make a diagnosis. Steroids, therefore, should be given only in an immediately life-threatening situation after consultation with a pediatric oncologist. Even more rarely, the mass may not be sensitive to corticosteroids, and emergent radiation therapy may be considered. 24