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Oncological emergencies
- 1. ONCOLOGICAL EMERGENCIES DR. VISHALKR. KANDHWAY Max Superspeciality Hospital, Patparganj
- 2. Complications of Mlignancy -Upper airway obstruction - Malignant pericardial tamponade - Superior vena cava syndrome - Acute spinal cord compression - Hypercalcemia - Hyperviscosity syndrome - Hyperleukocytic syndrome - Tumor lysis syndrome - SIADH - Adrenal insufficiency / crisis - Thrombocytopenia / hemorrage - Immunosuppression / infection
- 3. TLS • Metabolic consequensesresulting from sudden release of potassim, phosphates & purine metabolites from tumor cells undergoing cell death.
- 4. Pathogenesis • Chemotherapy isgiven to fast growing cells. This lysis causes a shift of intracellular components into the circulation, affecting the kidneys and causing dangerous electrolyte imbalances
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- 6. Risk factors Cancer type-ALL, Burkitts lymphoma Following chemotherapy,radiation, chemoembolisation Renal insufficiency Dehydration
- 7. Signs & Symptoms GI:nausea, vomiting, diarrhea Cardiac: dysrhythmias GU: flank pain, anuria, cloudy urine Neuro: seizures, altered mentation, stupor
- 8. TREATMENT HYDRATION • High rateof fluids – 200-300ml/hr • U.O. to be maintained @ 80-100ml/m2/h • Urine specific gravity to be maintained <1.01 • Most effective strategy for preventing urate induced obstructive uropathy LOOP DIURETICS • To maintain U.O. • Contraindicated in hypovolemia or obstructive uropathy
- 9. URINE ALKALANIZATION Controversial Can leadformation of urinary xanthine crystals May cause urinary obstruction ALLOPURINOL • Hypoxanthine analog that competitively inhibits xanthine oxidase • Dose 600mg/day if uric acid <8mg/dl • Start prior to chemo • Caution in renal impairment • Causes skin hypersensitivity reaction
- 10. RASBURICASE • Oxidizes preformeduric acid to allantoin which is highly soluble in urine • Used when uric acid level >8mg/dl • Dose-infusion 0.1-0.2mg/kg/day in 50 ml NS over 30 min for 5 days • Adverse reaction- anaphylaxis, rash, hemolysis Hyperkalemia • Increase excretion: IVF, diuretics, Kaexylate • Shift back into cells: IV insulin and dextrose Hypocalemia- Only treat if extremely low.
- 11. HYPERPHOSPHATEMIA •Phosphorus binder: aluminumhydroxide, Calcium carbonate, sevelamer hydroxide, lanthanum carbonate •Decrease oral intake HEMODIALYSIS • Volume overload • Serum uric acid >10mg/dl • Rapidly rising phosphorus • Uncontrolled hyperkalemia
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- 13. LEUCOSTASIS • Syndrome associatedwith high number of immature leukocytes(blasts) in peripheral circulation • High & rapidly rising blast counts usually >100,000/ml Associated malignancy • AML especially myelomonocytic(M4) & monocytic(M5) subtypes • CML in blast crisis • Rarely in ALL or CLL
- 14. Pathology: • Occlusive intravascularaggregates of blasts blocks microcirculation in multiple organs Symptoms: • Usually nonspecific • SOB • Headache • Confusion • Stupor • Focal neurologoical deficit
- 15. TREATMENT • Hydration • Hydroxyurea50-100mg/kg/day in 3 divided doses till blast count> 50,000/ml • Allopurinol and/or rasburicase • Leucopheresis till count< 50,000/ml • Definitive treatment for cancer Supportive Treatment: RBC transfusion to be restricted Correct DIC & thrombocytopenia Broad spectrum antibiotics
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- 17. HYPERCALCEMIA Pathogenesis: 3 mechanisms •Osteolytic metastases with local cytokine release • Tumor secretion of parathyroid hormone-related protein (PTHrP) • Tumor production of calcitriol
- 18. • Symptoms &Signs usually non-specific GI: • Constipation is most common • Anorexia • Vague abdominal pain
- 19. Renal dysfunction: Nephrolithiasis – Morecommon in hyperparathyroidism Nephrogenic diabetes insipidus – Defect in concentrating ability – Polyuria and polydipsia Chronic renal failure – Longstanding high calcium Calcifcation, degeneration, and necrosis of tubules
- 20. Neuropsychiatric: • Anxiety • Depression •Cognitive dysfunction – Delerium – Psychosis – Hallucinations – Somnolence – Coma CVS • Short QT interval • Supraventricualr arrhythmias • Ventricular arrhythmias
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- 23. SUPERIOR VENA CAVASYNDROME • Partial blockage or compression of blood flow in the superior vena cava results in signs and symptoms of SVC syndrome
- 25. Etiology: • Lung Cancer80% • Lymphoma 10% • Other Malignancy 5% • Benign causes 5% (e.g. aneurysm, goitre, fibrosis, infection etc.) Thrombosis Indwelling central venous catheters Subcutaneous tunneled catheters have fewer thrombotic and infectious complications
- 26. Symptoms & Signs Asthe obstruction develops venous collaterals are formed Symptom onset depends on speed of SVC obstruction onset Shortness of breath is the most common symptom Facial swelling or head fullness – exacerbated by bending forward or lying down Cough Arm edema Cyanosis
- 27. Physical findings: Venous distension –neck – chest wall
- 28. DIAGNOSIS Radiographic studies: • Mostpatients have an abnormal chest x-ray at presentation • Most common findings are – Mediastinal widening – Pleural effusion
- 29. CT Chest • Preferredchoice • IV contrast – defines the level of obstruction – Maps out collateral pathways – Can identify underlying cause of obstruction
- 30. Venography: • Bilateral upperarm venograpy – superior to CT to define site of obstruction – Does not define cause unless thrombosis is solely responsible
- 31. MRI: Can be usefulin patients with IV contrast allergies
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- 33. SPINAL CORD COMPRESSION •Neoplastic invasion of the space between vertebrae and spinal cord (epidural invasion) – Usually from bone metastases Causes • Metastatic tumor from any primary site • Prostate, breast, and lung carcinoma – 15-20% of cases • Renal cell, non-Hodgkin’s lymphoma, or myeloma – 5-10% of cases
- 34. Spinal Locations: • Thoracicspine: 60% • Lumbosacral spine: 30% • Cervical spine: 10%
- 35. Clinical Features Pain: • Usuallyfirst symptom – 80-90% of the time • Usually precedes other neurologic symptoms by several weeks – Increases in intensity • Severe local back pain • Aggravated by recumbency – Distension of venous plexus • May become radicular
- 36. Motor: • Weakness: 60-85% •At or above conus medularis – Extensors of the upper extremities • Above the thoracic spine – Affects flexors in the lower extremities • Patients may be hyperreflexic below the lesion and have extensor plantars • Weakness tends to be symmetrical • Progressive weakness is followed by loss of gait function then paralysis • The severity of weakness is greatest with thoracic metastases
- 37. Sensory: • Less commonthan motor findings • Still present in majority of cases • Ascending numbness and parathesias
- 38. Bowel & Bladder: •Loss is late finding • Autonomic neuropathy presents usually as urinary retension – Rarely sole finding
- 39. Radiological investigations: • CTmyelography involves a lumbar puncture – Contraindicated in brain metastases, thrombocytopenia, or coagulopathy – Can diagnose leptomeningeal metastases • MRI Images whole spine High detail Spares lumbar puncture Patients in pain must lie still
- 40. MRI of epiduralspinal cord compression in a women with past history of breast cancer.
- 41. Pain management: • Corticosteroids –Decrease edema • Opiates – Needed to decrease pain for comfort and examination purposes
- 42. Radiation therapy: • Relievespain in most cases • Post-neurological function usually determines response • Response most associated with tumor type and radiosensitivity; eg. lymphoma
- 43. Surgery: • Changing role •Recent controlled trial comparing aggressive surgery followed by radiation vs. radiation alone • Improvement in surgery + radiation therapy
- 44. Chemotherapy: • Can besuccessful in chemosensitive tumors – Hodgkin’s lymphoma – Non-Hodgkin’s lymphoma – Neuroblastoma – Germ cell – Breast cancer (hormonal manipulation) – Prostate cancer (hormonal manipulation)
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- 46. HYPERVISCOSITY SYNDROME • Refersto the clinical sequelae of increased blood viscosity. • Increased serum viscosity results from increased circulating serum immunoglobulins and can be seen in diseases like multiple myeloma. • HVS can also result from increased cellular blood components in hyperproliferative states such as leukemia, polycythemia & myloproliferative disorders.
- 47. Clinical Presentation: consistsof triad of mucosal bleeding, visual changes & neurologic symptoms. Pathophysiology: • Viscosity is a property of liquid & is described as the resistance that a liquid exibits to the flow of 1 layer over another. • As serum proteins or cellular components increase, the blood becomes more viscous. Vascular stasis & resultant hypoperfusion then lead to clinical symptoms of HVS. • HVS is associated most commonly with plasma cell dyscrasias & is due to the large size of IgM.
- 48. Labs: • Elevated serumviscosity (normal 1.4-1.8 centipoises) • CBC- rouleaux formation • WBC- 100,000/uL or greater • TP & albumin • Electrolytes: hypercalcemia, hyperphosphotemia & hyperkalemia • Coagulation profile • CXR, CT brain, MRI
- 49. Treatment: • Plasmapheresis isthe treatment of choice for initial management & stablization. • Other options are leukapheresis, plateletpheresis & phlebotomy
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